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Diabetes & perio

1. Diabetes is associated with increased risk and severity of periodontal disease like gingivitis and periodontitis. Poorly controlled diabetes is linked to worse periodontal inflammation and bone loss. 2. The mechanisms involve altered immune response in diabetes that impairs wound healing and increases susceptibility to oral infections. Hyperglycemia also influences the subgingival microbiome and increases non-enzymatic glycation end-products in tissues. 3. Studies found greater gingival bleeding, deeper pockets, more clinical attachment loss, and alveolar bone loss in people with diabetes compared to those without diabetes. Improving blood glucose control can help reduce periodontal inflammation in many cases.

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DIABETES MELLITUS AND PERIODONTIUM SANGEETA ROY PG 1ST YEAR
INTRODUCTION  Diabetes mellitus represents a spectrum of metabolic disorders & is 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 Alteration in lipid and protein metabolism  Result in the inability of glucose to be transported from the bloodstream into the tissues, which results in high blood glucose levels and excretion of sugar in the urine.
DIABETES MELLITUS  DEFINITION:  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.  Diabetes mellitus is a clinically & genetically heterogenous metabolic disease characterized by abnormally elevated blood glucose level & dysregulation of carbohydrate, protein & fat metabolism. Akintoye SO,2003
HISTORY  Diabetes was first described in an Egyptian manuscript from 1500 BC  The term diabetes was probably coined by Apollonius of Memphis around 250 BC,  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.  Sir Frederick Grant Banting, Charles Herbert Best introduced effective treatment—insulin injections and the first patient was treated in 1922
EPIDEMIOLOGY  According to International Diabetes Federation (2012), there are more than 371 million people in world who have diabetes  Almost half of them are unaware.
CLASSIFICATION  classification of diabetes by the American Diabetes Association in 2001
Etiologic classification byAmerican diabetic association (1997) CLASSIFICATION CHARACTERISTIC TYPE 1 DM β Cell destruction, leading to absolute insulin deficiency Immune mediated Idiopathic TYPE 2 DM Insulin resistance with relative insulin deficiency OTHER SPECIFIC TYPES OF DM Heterogenous group with partially known etiology Genetic defect of β cell function Genetic defect in insulin action Disease of exocrine pancreas Endocrinopathies Drug/ chemical induced Infection Immune mediated Other genetic syndrome GESTATIONAL DM Any degree of glucose intolerance with onset or first recognition during pregnancy
PATHOPHYSIOLOGY FOOD CONSUMPTION BREAKDOWN OF CARBOHYDRATE IN GIT ABSORPTION OF SUGAR IN BLOOD STREAM INCREASED BLOOD GLUCOSE LEVEL SECRETION OF INSULIN FROM β CELLS OF PANCREAS INSULIN BINDS TO TARGET CELL RECEPTORS ALLOW ENTRY OF GLUCOSE INTO CELL DECREASE BLOOD GLUCOSE LEVEL TYPE 1 DESTROY β CELLS TYPE 2 CAUSE RESISTENCE AT RECEPTOR & POST RECEPTOR LEVEL CARBOHYDRATE METABOLISM,INSULIN AND DIABETES
Type 1 DM pathophysiology Viral infection, autoimmune diseases (IMMUNE MEDIATED) Cellular mediated autoimmune destruction of β cells of pancreatic islets No/ decreased production of insulin Glucose entry into cell is inhibited More glucose in blood Hyperglycemia Unknown (IDIOPATHIC)
Type 2 DM pathophysiology Peripheral resistance to insulin Increased production of glucose by liver Insulin secretory defect of β cells Prevents its proper use at cellular level Excess glucose in blood stream Less entry of glucose in cells Hyperglycemia
Other specific type DM Genetic defect of β cell function, insulin action Less insulin Hyperglycemia
Gestational DM Increased insulin resistance Prevents its proper use at cellular level Excess glucose in blood flow Hyperglycemi a
 Deficiency of insulin secretion or insulin resistance results in Inability to transport glucose into cells Glucose retained in blood stream Hyperglycemia Complication
CHARACTERISTICS
CLASSIC SYMPTOMS
SIGNS & SYMPTOMS OF UNDIAGNOSED DIABETES CLINICAL FEATURE POLYDIPSIA POLYURIA POLYPHAGIA WT LOSS WEAKNESS, MALAISE NOCTURNAL ENURESIS IRRITABILITY DRY MOUTH CHRONIC SKIN INFECTION KETOACIDOSIS PERIODONTAL DISEASE CHANGE S IN VISION PRURITIS PARESTHESIA POSTURAL HYPOTENSION IMPOTENCE
DIAGNOSIS NORMAL IMPAIRED FASTING GLUCOSE DM FASTING GLUCOSE ‹110mg/dL 110- 126mg/dL ≥126mg/dL 2hr POSTPRANDI AL PLASMA GLUCOSE ‹140mg/dL 140- 200mg/dL ≥200mg/dL OGTT Plasma glucose at 2hr ≥200mg/dL
COMPLICATION SITES PRESENTATION EYES Retinopathy, Blindness KIDNEY Nephropathy, renal failure NERVOUS SYSTEM Peripheral & Cranial neuropathy(III,IV,VI,VII CN) SKIN & ORAL MUCOSA Infection & delayed wound healing PERIODONTIUM Gingivitis & Periodontitis CVS Atherosclerosis, ischemia, coronary artery disease
Microvascular and macrovascular complications  microvascular complications of retinopathy, nephropathy and neuropathy are specifically associated with diabetes,  risk of macrovascular disease is greatly increased in diabetic patients American diabetes association,2001
 Sustained hyperglycemia plays a primary role in both the onset and progression of visual impairment or blindness, kidney failure, limb amputation, stroke, and myocardial infarction Steinberg D,1997
Atherosclerosis Hyperglycemia alterations in lipid metabolism & nonenzymatic glycation of proteins i.e. collagen. altered function of cell membranes and changes in cell–cell and cell–matrix interactions. increased vessel wall thickness formation of atheromas and microthrombi in large vessels, alterations in endothelial cell function and vascular permeability in the microvasculature.
AGE proteins – (advanced glycation end- products )-modified collagen in vessel walls covalently cross-links with circulating low density lipoprotein atherosclerosis
Retinopathy, Nephropathy The glycation of proteins, lipids and nucleic acids in diabetic patients accumulation of these glycated proteins - advanced glycation end- products (AGEs) in the small blood vessels of endorgans i.e. retina, glomerulus, endoneurial region, and in the walls of large blood vessels Vlassara H,1994 increased basement membrane thickness in retina, around the nerves, thickening of mesangial matrix in the glomerulus, & accumulation of collagen in larger vessels. progressive narrowing of the vessel lumen decreased perfusion
Altered healing AGEs increased collagen cross-linking formation of highly stable collagen macromolecules that are resistant to normal enzymatic degradation and tissue turnover Brownlee M,1994
Effects at the cellular level A receptor for AGEs known as RAGE (receptor for AGE) has been identified on the surface of endothelial cells, neurons, smooth muscle cells, and monocytes/macrophages Schmidt AM,1996 Hyperglycemia increased expression of the receptor and increased AGE– RAGE interaction. increase in vascular permeability of endothelium & thrombus formation Ficara AJ,1975
AGEs are chemotactic for monocytes Interaction between AGEs RAGE, on monocyte/macrophage membranes induces increased cellular oxidant stress & activates the transcription factor NF-kB. This signals a change in the monocyte/macrophage phenotype increased production of proinflammatory cytokines such as IL-1 & TNF and growth factors i.e. platelet-derived growth factor and insulin-like growth factor Kiestein M,1992 chronic inflammatory process in atheroma formation.
CLASSIC COMPLICATION  1. Diabetic Retinopathy  2. Diabetic Neuropathy  3. Diabetic Nephropathy  4. Atherosclerosis  5. Impaired wound healing  6. Periodontal disease (Loe H 1993)
DIABETES & ORAL DISEASE Diabetes is associated with several oral conditions  alterations in salivary flow & constituents of saliva,  increased incidence of oral infection  burning mouth,  changes in wound healing,  Increased prevalence and severity of periodontal disease.
Salivary flow  Autonomic neuropathy, a complication of diabetes mellitus, may result in alteration of salivary secretion Meurman JH, 1998  In studies of type 2 diabetes mellitus subjects and non-diabetes mellitus controls, no significant differences in salivary flow rates or organic constituents of saliva were seen Meurman JH, 1998  Likewise, there were no differences in the prevalence of coronal caries or root caries Collin HL, 1998  The salivary counts of yeasts and of acidogenic streptococci and lactobacilli were also similar between the groups.
xerostomia  Xerostomia and parotid gland enlargement may occur in people with diabetes, and may be related to the degree of glycemic control COLLIN HL 2000  Xerostomia may be associated with sensation of burning mouth & tongue ,cheilosis, mucosal drying , craking
 Many diabetic patients have conditions other than diabetes for which they are medicated, and many of these medications produce xerostomia as a side effect.  However, the effect of xerostomic medications on salivary flow rates was greater in diabetic individuals than in control patients. MEURMAN JH 1998
candidiasis  Fungal infections i.e. candidiasis may increase on dry mucosa Fisher BM,1987  Guggenheimer et al. 2000 found 15.1% of 405 type 1 diabetes mellitus subjects had candidiasis, compared to only 3.0% of 268 non-diabetes mellitus control subjects.  Multivariate regression analysis found presence of Candida hyphae to be significantly related to poor glycemic control.
caries  Studies have shown an increased caries rates in diabetes mellitus Jones RB,1992; others have demonstrated similar or lower caries incidence Tenovuo J,1986  decreased salivation or increased glucose concentrations in saliva and gingival crevicular fluid account for an increased caries risk.  However, most diabetic patients limit their fermentable carbohydrate intake, and this less cariogenic diet may decrease caries risk.
Oral microflora  Alteration in flora due to increased glucose in GCF & blood.  Cause change in environment of flora & qualitative changes in bacteria  Results in periodontal destruction.  Predominance of Candida albicans, Hemolytic streptococci ,staphylococci.
Microorganism in pt with IDDM  Capnocytophaga, anaerobic virios, Actinomyces sp. Black pigmented bacteroid Mascola B,1970  Porphyromonus gingivalis, P. intermedia, Actinobacillus actinomycetemcomitans are less Gusberti F,1982
Microorganism in pt with NIDDM  P. gingivalis, P. intermedia, Campylobacter rectus are predominent. Genco RJ,1987
Infection  Increased susceptibility to infection  Due to polymorphonuclear leukocyte deficiencies  Results in impaired chemotaxis, defective phagocytosis, impaired adherence McMullen JA,1981
In poorly controlled diabetic pt  Impaired PMNs, monocyte/macrophages Iacopino AM,2001  Diminished primary defense  Unchecked bacterial proliferation  No change in IgA, IgM, IgG Robertson HD,1974
Effect on gingiva  Tendency towards enlarged gingiva, sessile/ pedunculated gingival polyp, polypoid gingival proliferation, abcess, periodontitis , mobility of teeth. Hirschfeld I, 1934
PERIODONTAL MANIFESTATIONS  Tendency towards enlarged gingiva.  Sessile/pedunculated gingival polyps.  Polypoid gingival proliferations  Abscess formation  Periodontitis  Loosened teeth - Hirchfeld I (1934)
GINGIVITIS  Diabetes is associated with increased prevalence and severity of gingivitis.  Children before puberty with poorly controlled type 1 diabetes mellitus had a higher incidence and severity of gingival inflammation than controlled children. Gusberti et al. 1983  Cianciola et al.1982 Confirmed an increase in gingivitis in type 1 diabetes mellitus children after the age of 11
 poorly controlled diabetes mellitus children has higher levels of gingival inflammation regardless of plaque levels. Firalti E. 1997  Improvement in glycemic control decreases signs of gingival inflammation Karjalainen k.1996  Guthmiller et al. 2001 found greater gingival inflammation in pregnant women with type 1 diabetes mellitus than in pregnant women without diabetes mellitus.
 Cutler et al. 1999 demonstrated greater gingival inflammation in type 2 diabetes mellitus adults than controls  Bridges et al. 1996 found no relationship between gingivitis and level of glycemic control.  These studies show -presence of diabetes mellitus is often, but not always associated with increased gingival inflammation  level of glycemic control may play a role in the gingival response to bacterial plaque in many individuals. Mealey & Moritz ,2003
Probing depth & clinical attachment loss  Firalti et al. 1996 found increased probing depth and clinical attachment loss, when compared to age- and sex-matched control subjects.  mean attachment loss and bone loss scores are twice in 15-34 yrs diabetic pt than same aged non diabetes mellitus subjects.
 Type 1 DM subjects with poor metabolic control over 2–5 years has greater prevalence of deep probing depths and advanced attachment loss. Tervonen & Oliver 1993  There is increasing prevalence of deeper pockets as metabolic control worsened. Tervonen & Knuuttila 1986
Gingival Bleeding  Significantly greater gingival bleeding in poorly controlled patients Ervasti et al. 1984  Number of bleeding sites decreased as glycemic control improved.
Periodontitis  more severe periodontal condition in type 2 diabetic adults Papapanou 1996  In younger individuals, type 1 diabetes mellitus is associated with an increased risk of periodontitis Brian L.2003  Cianciola et al. 1982 found no periodontitis among the diabetes mellitus subjects under the age of 12.
 Between ages 13 and 18, 13.6% of the individuals had periodontitis.  Individuals from 19 to 32 years old had a prevalence of 39%.  The most significant risk factors for periodontitis are age, presence of calculus, and presence of type 2 diabetes mellitus. Bridges RB, 1996
Bone loss  Type 2 diabetes mellitus is associated with significantly increased risk of progressive bone loss. Taylor GW,1998  There is increasing prevalence of alveolar bone loss as glycemic control worsened.  The mean percentage of sites with > 15% bone loss went from 28% in well controlled type 1 diabetes mellitus subjects to 44% in poorly controlled subjects. Tervonen et al. 2000
Factors Contributing to Development of Periodontal Disease Polymorphonuclear leukocyte function Collagen Metabolism & 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  Reduced collagen maturation  Collagen homeostasis is Affected  GCF collagenase activity increased
INFECTION Mainly due to: • Impaired defence mechanism 1. Defects in PMN function 2. Induction of insulin resistance 3. Vascular changes Hyperglycemic state Glycosylation of basement membrane, proteins • Thickning of gingival capillaries, • Disruption of BM Swelling of Endothelium 1. Oxygen diffusion 2. Metabolic waste elimination 3. PMN Migration 4. Diffusion of serum factors Impeded
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
BACTERIAL ASSOCIATION  Glucose content of GCF & blood is higher in diabetics.  Results in changed environment for the microflora & Presence of higher levels of specific microorganisms such as Actinobacillus actinomycetemcomitans & Capnocytophaga Mashimo et al 1983  The proportion of P gingivalis was reported to be higher in noninsulin- dependent diabetes mellitus patients with periodontitis.  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
MECHANISM OF INTERACTION
CHANGES IN SUBGINGIVAL ENVIRONMENT
Alterations in subgingival microbiota  Deepening of periodontal pockets & shift to a flora predominated by gram-negative rods and filaments. Mc Namara Tf, 1981  increase in proportions of Capnocytophaga species, while Fusobacterium and Bacteroides species remained at low levels. Masimo PA, 1983  High proportions of Prevotella intermedia were also found in diseased sites Sastrowijoto S ,1989
 increased prevalence of Porphyromonas gingivalis in type 1 diabetes mellitus subjects Thorstenson H, 1995  Type 2 diabetes mellitus subjects with periodontitis have fairly similar microbiota to non-diabetes mellitus periodontitis patients,  different serotype of P. gingivalis were found in diabetes mellitus subjects. Zambon et al. ,1988
Change in gingival crevicular fluid composition  Increased glucose levels in gingival crevicular fluid  decreased chemotaxis of periodontal ligament fibroblasts in response to platelet-derived growth factor. Nishimura et al. Nashimura F,1998  adversely affect periodontal wound healing and the local host response to microbial challenge.
ALTERED TISSUE HOMEOSTASIS AND WOUND HEALING
Decreased collagen production  Changes in collagen synthesis, maturation, and turnover  Contribute to alterations in wound healing and to periodontal disease initiation and progression. Weringer EJ, 1981  The rate of collagen production can be restored by administration of insulin to normalize blood glucose levels Ramamurthy NS, 1983
Increased matrix metalloproteinase activity  Decreased synthesis, newly formed collagen is susceptible to degradation by collagenase( source is neutrophil), a matrix metalloproteinase which is elevated in diabetic tissues, including the periodontium Golub LM, 1978  Use of tetracycline antibiotics results in a reduction in collagenase production Golub LM, 1982
Accumulation of advanced glycation endproducts (AGEs)  decreased collagen production and increased collagenase activity, collagen metabolism is altered by accumulation of AGEs in the periodontium.  Changes affecting the blood vessels of the periodontium, and these changes are related to AGE formation.  Increased thickness of gingival capillary endothelial cell basement membranes and the walls of small blood vessels Frantzis TG, 1971
 This thickening impair exchange of oxygen and metabolic waste products across the basement membrane.  two-fold increase in accumulation of AGEs in the periodontium Schmidt et al. Schimidt AM,1996
 Increased oxidant stress  widespread vascular injury  AGE formation also stimulates proliferation of arterial smooth muscle cells, increasing thickness of vessel walls and decreasing the vessel lumen.
Decreased tissue turnover  AGE accumulation results in increased cross-linking of collagen, reducing collagen solubility and decreasing turnover rate Brownlee M ,1994  greater degradation of newly formed, more soluble collagen.  greater cross-linking of mature collagen.
 In the capillaries, this accumulation of highly cross-linked collagen in the basement membrane increases membrane thickness  Alter the tissue response to periodontal pathogens, resulting in increased severity and progression of periodontitis.
Changes in host immunoinflammatory response
Decreased polymorphonuclear leukocyte chemotaxis, adherence, phagocytosis  The polymorphonuclear leukocyte plays a major role in maintaining a healthy periodontium in the face of periodontopathic microorganisms  reduction in polymorphonuclear leukocyte function, including chemotaxis, adherence and phagocytosis Hill HR, 1974  May be associated with defect of genetic component Leeper SH,1985
 Chemotaxis may be improved in those with better glycemic control  Defects affecting polymorpho nuclear leukocytes, the first line of defense against subgingival microbial agents, may result in significantly increased tissue destruction.
Elevated pro-inflammatory cytokine response from monocytes/macrophages  hyper-responsive monocyte/macrophage phenotype in which stimulation by bacterial antigens such as lipopolysaccharide results in dramatically increased pro-inflammatory cytokine production  increased production of tumor necrosis factor-α by monocytes Salvi et al. Salvi CE, 1997
 When challenged with lipopolysaccharide from P. gingivalis, diabetic monocytes showed a 24–32-fold increased production of tumor necrosis factor- α  Production of prostaglandin E2 and interleukin-1b was also significantly higher
Increased tissue oxidant stress  people with diabetes mellitus have a hyperresponsive monocyte/macrophage phenotype, and it is likely that there is a genetic component to this phenomenon (135).  AGE formation plays an important role in upregulation of the monocyte/macrophage cell line.  Accumulation of AGEs in the periodontium stimulates migration of monocytes to the site.
 AGE–RAGE interaction results in immobilization of monocytes at the local site.  induces a change in monocyte phenotype, upregulating the cell and significantlymincreasing pro-inflammatory cytokine production.  increased gingival crevicularfluid production oftumor necrosis factor-a, prostaglandin E2 and interleukin-1b 159
 This interaction also increases oxidant stress within the tissue, resulting in tissue destruction (166).  blocking the receptor RAGE decreases levels of the pro-inflammatory cytokines tumor necrosis factor- a and IL-6 in gingival tissues, decreases levels of tissue-destructive matrix metalloproteinases, lowers AGE accumulation in periodontal tissues and decreases alveolar bone loss in response to P. gingivalis (89).
Pathogenesis
2- WAY RELATIONSHIP BETWEEN PERIODONTAL DISEASE AND DM
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
AUTHOR YEAR STUDY 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. Sastrowijo t o S et al 1990 Improvement in glycemic control may be associated with decreased gingival inflammation. Papapano u 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 nondiabetic 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 PERIODONTITIS ON DM  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.
AUTHOR YEAR STUDY 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 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 & root planing alone compared to diabetic subjects treated with SRP plus systemic amoxicillin/clavulanic acid. Promsudt hi A et al 2005 In older, poorly controlled type 2 diabetic subjects who received SRP 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 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.  longitudinal studies of various periodontal treatment modalities are needed to determine the healing response in individuals with diabetes compared to individuals without diabetes. Grossi SG,1996
MANAGEMENT OF DIABETES 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 MANAGEMENT
ANTI AGE THERAPY  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 CONDIDERATION  Patients with well-controlled diabetes can 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 TREATEMENT  Patients with well controlled DM can be treated similarly to non-diabetic patients for most routine dental needs.  Keep appointments short, atraumatic, and stressfree  morning appointments  Use appropriate vasoconstrictor agents  For stressful procedures the usual drug regime may be altered
Response to periodontal treatment in patients with diabetes  Well controlled diabetes mellitus subjects with moderate to advancedmperiodontal disease, scaling and root planing resulted in similar clinical changes when compared to non-diabetes mellitus subjects 25  Conversely, poorly controlled diabetes mellitus patients often have a less favorable response to treatment
 initial response to scaling and root planing was good , but the incidence of disease recurrence over the subsequent 12 months was greater in poorly controlled diabetes mellitus Individuals Tervonen et al. (188)  At the 5-year re-evaluation, diabetes mellitus patients had a similar percentage of sites gaining or losing attachment, and a similar percentage of sites with stable attachment levels, compared to non- diabetes mellitus subjects
USE OF ANTIBIOTIC  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.
IMPLANT PLACEMENT CONSIDERATION  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 EMERGENCY  Hypoglycemic crisis  Hyperglycemic crisis
HYPOGLYCEMIC CRISIS  INSULIN SHOCK  Blood glucose level <60 mg/dl  Signs: sweating , tremor, dizziness, headache, loss of consciousness  Treatment : 1. recognition of hypoglycemia 2. Termination of dental procedure 3. Position- upright 4. A-B-C 5. D-definitive care – administration of oral carbohydrate (3-4 tspn of sugar/ candy)
HYPERGLYCEMIC CRISIS  Dental pt with hyperglycemia represent ASA IV risk & shouldn’t receive any dental t/t.  In unconscious pt; 1.Terminate dental procedure 2.Position - trendenlenburg 3.A-B-C 4.D- definitive care- 5% dextrose & H2O/ NS, administration of O2
SPECIFIC MANAGEMENT GUIDELINES  USE OF EPINEPHRINE  Under stressful situation production of epinephrine & cortisol increases -> increase blood glucose level -> adequate pain control & stress reduction  Epinephrine is not contraindicated for LA
PERIODONTAL MANAGEMENT  Periodontal t/t must be conducted in parallel with DM t/t. Taylor GW,1999  Primary t/t should be nonsurgical  Surgical t/t should be done in well glycemic controlled (100-200 mg/dl) pt , medication should be modified, it can result in prologed healing. Kripal K,2017
 Combination of nonsurgical debridement & systemic antibiotic has shown better result in advance periodontitis cases Mealey BL, 2006  Combination of tetracycline & doxycycline with SRP also resulted better than SRP alone , even for topical intrasulcular doxycycline also resulted better Ship JA,2003
 These drugs inhibit MMPs, gcf collagenase, risk of bacterial resistance, bone resorption, bone loss.  Supportive periodontal therapy should be provided at intervals of 2-3 months.
GUIDENINES FOR TREATEMENT  DIABETES & PERIODONTAL DISEASE: CENSUS REPORT OF THE JOINT EFP/AAP WORKSHOP ON PERIODONTITIS & SYSTEMIC DISEASES  (CHAPPLE LC,GENCO R. J PERIODONTOL 2013)
GUIDELINE- A  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  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  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  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.

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Diabetes & perio

  • 1.
  • 2.
    INTRODUCTION  Diabetes mellitusrepresents a spectrum of metabolic disorders & is 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 Alteration in lipid and protein metabolism  Result in the inability of glucose to be transported from the bloodstream into the tissues, which results in high blood glucose levels and excretion of sugar in the urine.
  • 3.
    DIABETES MELLITUS  DEFINITION: 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.  Diabetes mellitus is a clinically & genetically heterogenous metabolic disease characterized by abnormally elevated blood glucose level & dysregulation of carbohydrate, protein & fat metabolism. Akintoye SO,2003
  • 4.
    HISTORY  Diabetes wasfirst described in an Egyptian manuscript from 1500 BC  The term diabetes was probably coined by Apollonius of Memphis around 250 BC,  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.  Sir Frederick Grant Banting, Charles Herbert Best introduced effective treatment—insulin injections and the first patient was treated in 1922
  • 5.
    EPIDEMIOLOGY  According toInternational Diabetes Federation (2012), there are more than 371 million people in world who have diabetes  Almost half of them are unaware.
  • 7.
    CLASSIFICATION  classification ofdiabetes by the American Diabetes Association in 2001
  • 8.
    Etiologic classification byAmericandiabetic association (1997) CLASSIFICATION CHARACTERISTIC TYPE 1 DM β Cell destruction, leading to absolute insulin deficiency Immune mediated Idiopathic TYPE 2 DM Insulin resistance with relative insulin deficiency OTHER SPECIFIC TYPES OF DM Heterogenous group with partially known etiology Genetic defect of β cell function Genetic defect in insulin action Disease of exocrine pancreas Endocrinopathies Drug/ chemical induced Infection Immune mediated Other genetic syndrome GESTATIONAL DM Any degree of glucose intolerance with onset or first recognition during pregnancy
  • 9.
    PATHOPHYSIOLOGY FOOD CONSUMPTION BREAKDOWN OFCARBOHYDRATE IN GIT ABSORPTION OF SUGAR IN BLOOD STREAM INCREASED BLOOD GLUCOSE LEVEL SECRETION OF INSULIN FROM β CELLS OF PANCREAS INSULIN BINDS TO TARGET CELL RECEPTORS ALLOW ENTRY OF GLUCOSE INTO CELL DECREASE BLOOD GLUCOSE LEVEL TYPE 1 DESTROY β CELLS TYPE 2 CAUSE RESISTENCE AT RECEPTOR & POST RECEPTOR LEVEL CARBOHYDRATE METABOLISM,INSULIN AND DIABETES
  • 10.
    Type 1 DMpathophysiology Viral infection, autoimmune diseases (IMMUNE MEDIATED) Cellular mediated autoimmune destruction of β cells of pancreatic islets No/ decreased production of insulin Glucose entry into cell is inhibited More glucose in blood Hyperglycemia Unknown (IDIOPATHIC)
  • 11.
    Type 2 DMpathophysiology Peripheral resistance to insulin Increased production of glucose by liver Insulin secretory defect of β cells Prevents its proper use at cellular level Excess glucose in blood stream Less entry of glucose in cells Hyperglycemia
  • 12.
    Other specific typeDM Genetic defect of β cell function, insulin action Less insulin Hyperglycemia
  • 13.
    Gestational DM Increased insulin resistance Prevents its properuse at cellular level Excess glucose in blood flow Hyperglycemi a
  • 14.
     Deficiency ofinsulin secretion or insulin resistance results in Inability to transport glucose into cells Glucose retained in blood stream Hyperglycemia Complication
  • 15.
  • 16.
  • 17.
    SIGNS & SYMPTOMS OF UNDIAGNOSED DIABETES CLINICALFEATURE POLYDIPSIA POLYURIA POLYPHAGIA WT LOSS WEAKNESS, MALAISE NOCTURNAL ENURESIS IRRITABILITY DRY MOUTH CHRONIC SKIN INFECTION KETOACIDOSIS PERIODONTAL DISEASE CHANGE S IN VISION PRURITIS PARESTHESIA POSTURAL HYPOTENSION IMPOTENCE
  • 18.
    DIAGNOSIS NORMAL IMPAIRED FASTING GLUCOSE DM FASTING GLUCOSE ‹110mg/dL 110- 126mg/dL ≥126mg/dL 2hr POSTPRANDI ALPLASMA GLUCOSE ‹140mg/dL 140- 200mg/dL ≥200mg/dL OGTT Plasma glucose at 2hr ≥200mg/dL
  • 20.
    COMPLICATION SITES PRESENTATION EYES Retinopathy,Blindness KIDNEY Nephropathy, renal failure NERVOUS SYSTEM Peripheral & Cranial neuropathy(III,IV,VI,VII CN) SKIN & ORAL MUCOSA Infection & delayed wound healing PERIODONTIUM Gingivitis & Periodontitis CVS Atherosclerosis, ischemia, coronary artery disease
  • 21.
    Microvascular and macrovascularcomplications  microvascular complications of retinopathy, nephropathy and neuropathy are specifically associated with diabetes,  risk of macrovascular disease is greatly increased in diabetic patients American diabetes association,2001
  • 22.
     Sustained hyperglycemiaplays a primary role in both the onset and progression of visual impairment or blindness, kidney failure, limb amputation, stroke, and myocardial infarction Steinberg D,1997
  • 23.
    Atherosclerosis Hyperglycemia alterations in lipidmetabolism & nonenzymatic glycation of proteins i.e. collagen. altered function of cell membranes and changes in cell–cell and cell–matrix interactions. increased vessel wall thickness formation of atheromas and microthrombi in large vessels, alterations in endothelial cell function and vascular permeability in the microvasculature.
  • 24.
    AGE proteins –(advanced glycation end- products )-modified collagen in vessel walls covalently cross-links with circulating low density lipoprotein atherosclerosis
  • 25.
    Retinopathy, Nephropathy The glycationof proteins, lipids and nucleic acids in diabetic patients accumulation of these glycated proteins - advanced glycation end- products (AGEs) in the small blood vessels of endorgans i.e. retina, glomerulus, endoneurial region, and in the walls of large blood vessels Vlassara H,1994 increased basement membrane thickness in retina, around the nerves, thickening of mesangial matrix in the glomerulus, & accumulation of collagen in larger vessels. progressive narrowing of the vessel lumen decreased perfusion
  • 26.
    Altered healing AGEs increased collagencross-linking formation of highly stable collagen macromolecules that are resistant to normal enzymatic degradation and tissue turnover Brownlee M,1994
  • 27.
    Effects at thecellular level A receptor for AGEs known as RAGE (receptor for AGE) has been identified on the surface of endothelial cells, neurons, smooth muscle cells, and monocytes/macrophages Schmidt AM,1996 Hyperglycemia increased expression of the receptor and increased AGE– RAGE interaction. increase in vascular permeability of endothelium & thrombus formation Ficara AJ,1975
  • 28.
    AGEs are chemotacticfor monocytes Interaction between AGEs RAGE, on monocyte/macrophage membranes induces increased cellular oxidant stress & activates the transcription factor NF-kB. This signals a change in the monocyte/macrophage phenotype increased production of proinflammatory cytokines such as IL-1 & TNF and growth factors i.e. platelet-derived growth factor and insulin-like growth factor Kiestein M,1992 chronic inflammatory process in atheroma formation.
  • 29.
    CLASSIC COMPLICATION  1.Diabetic Retinopathy  2. Diabetic Neuropathy  3. Diabetic Nephropathy  4. Atherosclerosis  5. Impaired wound healing  6. Periodontal disease (Loe H 1993)
  • 30.
    DIABETES & ORALDISEASE Diabetes is associated with several oral conditions  alterations in salivary flow & constituents of saliva,  increased incidence of oral infection  burning mouth,  changes in wound healing,  Increased prevalence and severity of periodontal disease.
  • 31.
    Salivary flow  Autonomicneuropathy, a complication of diabetes mellitus, may result in alteration of salivary secretion Meurman JH, 1998  In studies of type 2 diabetes mellitus subjects and non-diabetes mellitus controls, no significant differences in salivary flow rates or organic constituents of saliva were seen Meurman JH, 1998  Likewise, there were no differences in the prevalence of coronal caries or root caries Collin HL, 1998  The salivary counts of yeasts and of acidogenic streptococci and lactobacilli were also similar between the groups.
  • 32.
    xerostomia  Xerostomia andparotid gland enlargement may occur in people with diabetes, and may be related to the degree of glycemic control COLLIN HL 2000  Xerostomia may be associated with sensation of burning mouth & tongue ,cheilosis, mucosal drying , craking
  • 33.
     Many diabeticpatients have conditions other than diabetes for which they are medicated, and many of these medications produce xerostomia as a side effect.  However, the effect of xerostomic medications on salivary flow rates was greater in diabetic individuals than in control patients. MEURMAN JH 1998
  • 34.
    candidiasis  Fungal infectionsi.e. candidiasis may increase on dry mucosa Fisher BM,1987  Guggenheimer et al. 2000 found 15.1% of 405 type 1 diabetes mellitus subjects had candidiasis, compared to only 3.0% of 268 non-diabetes mellitus control subjects.  Multivariate regression analysis found presence of Candida hyphae to be significantly related to poor glycemic control.
  • 35.
    caries  Studies haveshown an increased caries rates in diabetes mellitus Jones RB,1992; others have demonstrated similar or lower caries incidence Tenovuo J,1986  decreased salivation or increased glucose concentrations in saliva and gingival crevicular fluid account for an increased caries risk.  However, most diabetic patients limit their fermentable carbohydrate intake, and this less cariogenic diet may decrease caries risk.
  • 36.
    Oral microflora  Alterationin flora due to increased glucose in GCF & blood.  Cause change in environment of flora & qualitative changes in bacteria  Results in periodontal destruction.  Predominance of Candida albicans, Hemolytic streptococci ,staphylococci.
  • 37.
    Microorganism in ptwith IDDM  Capnocytophaga, anaerobic virios, Actinomyces sp. Black pigmented bacteroid Mascola B,1970  Porphyromonus gingivalis, P. intermedia, Actinobacillus actinomycetemcomitans are less Gusberti F,1982
  • 38.
    Microorganism in ptwith NIDDM  P. gingivalis, P. intermedia, Campylobacter rectus are predominent. Genco RJ,1987
  • 39.
    Infection  Increased susceptibilityto infection  Due to polymorphonuclear leukocyte deficiencies  Results in impaired chemotaxis, defective phagocytosis, impaired adherence McMullen JA,1981
  • 40.
    In poorly controlleddiabetic pt  Impaired PMNs, monocyte/macrophages Iacopino AM,2001  Diminished primary defense  Unchecked bacterial proliferation  No change in IgA, IgM, IgG Robertson HD,1974
  • 41.
    Effect on gingiva Tendency towards enlarged gingiva, sessile/ pedunculated gingival polyp, polypoid gingival proliferation, abcess, periodontitis , mobility of teeth. Hirschfeld I, 1934
  • 42.
    PERIODONTAL MANIFESTATIONS  Tendencytowards enlarged gingiva.  Sessile/pedunculated gingival polyps.  Polypoid gingival proliferations  Abscess formation  Periodontitis  Loosened teeth - Hirchfeld I (1934)
  • 45.
    GINGIVITIS  Diabetes isassociated with increased prevalence and severity of gingivitis.  Children before puberty with poorly controlled type 1 diabetes mellitus had a higher incidence and severity of gingival inflammation than controlled children. Gusberti et al. 1983  Cianciola et al.1982 Confirmed an increase in gingivitis in type 1 diabetes mellitus children after the age of 11
  • 46.
     poorly controlleddiabetes mellitus children has higher levels of gingival inflammation regardless of plaque levels. Firalti E. 1997  Improvement in glycemic control decreases signs of gingival inflammation Karjalainen k.1996  Guthmiller et al. 2001 found greater gingival inflammation in pregnant women with type 1 diabetes mellitus than in pregnant women without diabetes mellitus.
  • 47.
     Cutler etal. 1999 demonstrated greater gingival inflammation in type 2 diabetes mellitus adults than controls  Bridges et al. 1996 found no relationship between gingivitis and level of glycemic control.  These studies show -presence of diabetes mellitus is often, but not always associated with increased gingival inflammation  level of glycemic control may play a role in the gingival response to bacterial plaque in many individuals. Mealey & Moritz ,2003
  • 49.
    Probing depth &clinical attachment loss  Firalti et al. 1996 found increased probing depth and clinical attachment loss, when compared to age- and sex-matched control subjects.  mean attachment loss and bone loss scores are twice in 15-34 yrs diabetic pt than same aged non diabetes mellitus subjects.
  • 50.
     Type 1DM subjects with poor metabolic control over 2–5 years has greater prevalence of deep probing depths and advanced attachment loss. Tervonen & Oliver 1993  There is increasing prevalence of deeper pockets as metabolic control worsened. Tervonen & Knuuttila 1986
  • 51.
    Gingival Bleeding  Significantlygreater gingival bleeding in poorly controlled patients Ervasti et al. 1984  Number of bleeding sites decreased as glycemic control improved.
  • 54.
    Periodontitis  more severeperiodontal condition in type 2 diabetic adults Papapanou 1996  In younger individuals, type 1 diabetes mellitus is associated with an increased risk of periodontitis Brian L.2003  Cianciola et al. 1982 found no periodontitis among the diabetes mellitus subjects under the age of 12.
  • 55.
     Between ages13 and 18, 13.6% of the individuals had periodontitis.  Individuals from 19 to 32 years old had a prevalence of 39%.  The most significant risk factors for periodontitis are age, presence of calculus, and presence of type 2 diabetes mellitus. Bridges RB, 1996
  • 57.
    Bone loss  Type2 diabetes mellitus is associated with significantly increased risk of progressive bone loss. Taylor GW,1998  There is increasing prevalence of alveolar bone loss as glycemic control worsened.  The mean percentage of sites with > 15% bone loss went from 28% in well controlled type 1 diabetes mellitus subjects to 44% in poorly controlled subjects. Tervonen et al. 2000
  • 60.
    Factors Contributing to Developmentof Periodontal Disease Polymorphonuclear leukocyte function Collagen Metabolism & Advanced glycation end products Infections in patients with diabetes Wound healing Bacterial Associations
  • 61.
    POLYMORPHONUCLEAR LEUKOCYTE FUNCTION  ImpairedChemotaxis & adherence  Defective Phagocytosis  Diminished primary defense against periodontal pathogens.
  • 62.
    COLLAGEN METABOLISM  Reducedsynthesis of collagen & glycosaminoglycans  Reduced collagen maturation  Collagen homeostasis is Affected  GCF collagenase activity increased
  • 63.
    INFECTION Mainly due to: •Impaired defence mechanism 1. Defects in PMN function 2. Induction of insulin resistance 3. Vascular changes Hyperglycemic state Glycosylation of basement membrane, proteins • Thickning of gingival capillaries, • Disruption of BM Swelling of Endothelium 1. Oxygen diffusion 2. Metabolic waste elimination 3. PMN Migration 4. Diffusion of serum factors Impeded
  • 64.
    WOUND HEALING  WoundHealing 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
  • 65.
    BACTERIAL ASSOCIATION  Glucosecontent of GCF & blood is higher in diabetics.  Results in changed environment for the microflora & Presence of higher levels of specific microorganisms such as Actinobacillus actinomycetemcomitans & Capnocytophaga Mashimo et al 1983  The proportion of P gingivalis was reported to be higher in noninsulin- dependent diabetes mellitus patients with periodontitis.  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
  • 66.
  • 67.
  • 68.
    Alterations in subgingival microbiota Deepening of periodontal pockets & shift to a flora predominated by gram-negative rods and filaments. Mc Namara Tf, 1981  increase in proportions of Capnocytophaga species, while Fusobacterium and Bacteroides species remained at low levels. Masimo PA, 1983  High proportions of Prevotella intermedia were also found in diseased sites Sastrowijoto S ,1989
  • 69.
     increased prevalenceof Porphyromonas gingivalis in type 1 diabetes mellitus subjects Thorstenson H, 1995  Type 2 diabetes mellitus subjects with periodontitis have fairly similar microbiota to non-diabetes mellitus periodontitis patients,  different serotype of P. gingivalis were found in diabetes mellitus subjects. Zambon et al. ,1988
  • 70.
    Change in gingivalcrevicular fluid composition  Increased glucose levels in gingival crevicular fluid  decreased chemotaxis of periodontal ligament fibroblasts in response to platelet-derived growth factor. Nishimura et al. Nashimura F,1998  adversely affect periodontal wound healing and the local host response to microbial challenge.
  • 71.
  • 72.
    Decreased collagen production Changes in collagen synthesis, maturation, and turnover  Contribute to alterations in wound healing and to periodontal disease initiation and progression. Weringer EJ, 1981  The rate of collagen production can be restored by administration of insulin to normalize blood glucose levels Ramamurthy NS, 1983
  • 73.
    Increased matrix metalloproteinase activity Decreased synthesis, newly formed collagen is susceptible to degradation by collagenase( source is neutrophil), a matrix metalloproteinase which is elevated in diabetic tissues, including the periodontium Golub LM, 1978  Use of tetracycline antibiotics results in a reduction in collagenase production Golub LM, 1982
  • 74.
    Accumulation of advanced glycationendproducts (AGEs)  decreased collagen production and increased collagenase activity, collagen metabolism is altered by accumulation of AGEs in the periodontium.  Changes affecting the blood vessels of the periodontium, and these changes are related to AGE formation.  Increased thickness of gingival capillary endothelial cell basement membranes and the walls of small blood vessels Frantzis TG, 1971
  • 75.
     This thickeningimpair exchange of oxygen and metabolic waste products across the basement membrane.  two-fold increase in accumulation of AGEs in the periodontium Schmidt et al. Schimidt AM,1996
  • 76.
     Increased oxidantstress  widespread vascular injury  AGE formation also stimulates proliferation of arterial smooth muscle cells, increasing thickness of vessel walls and decreasing the vessel lumen.
  • 77.
    Decreased tissue turnover AGE accumulation results in increased cross-linking of collagen, reducing collagen solubility and decreasing turnover rate Brownlee M ,1994  greater degradation of newly formed, more soluble collagen.  greater cross-linking of mature collagen.
  • 78.
     In thecapillaries, this accumulation of highly cross-linked collagen in the basement membrane increases membrane thickness  Alter the tissue response to periodontal pathogens, resulting in increased severity and progression of periodontitis.
  • 79.
  • 80.
    Decreased polymorphonuclear leukocyte chemotaxis,adherence, phagocytosis  The polymorphonuclear leukocyte plays a major role in maintaining a healthy periodontium in the face of periodontopathic microorganisms  reduction in polymorphonuclear leukocyte function, including chemotaxis, adherence and phagocytosis Hill HR, 1974  May be associated with defect of genetic component Leeper SH,1985
  • 81.
     Chemotaxis maybe improved in those with better glycemic control  Defects affecting polymorpho nuclear leukocytes, the first line of defense against subgingival microbial agents, may result in significantly increased tissue destruction.
  • 82.
    Elevated pro-inflammatory cytokine responsefrom monocytes/macrophages  hyper-responsive monocyte/macrophage phenotype in which stimulation by bacterial antigens such as lipopolysaccharide results in dramatically increased pro-inflammatory cytokine production  increased production of tumor necrosis factor-α by monocytes Salvi et al. Salvi CE, 1997
  • 83.
     When challengedwith lipopolysaccharide from P. gingivalis, diabetic monocytes showed a 24–32-fold increased production of tumor necrosis factor- α  Production of prostaglandin E2 and interleukin-1b was also significantly higher
  • 84.
    Increased tissue oxidantstress  people with diabetes mellitus have a hyperresponsive monocyte/macrophage phenotype, and it is likely that there is a genetic component to this phenomenon (135).  AGE formation plays an important role in upregulation of the monocyte/macrophage cell line.  Accumulation of AGEs in the periodontium stimulates migration of monocytes to the site.
  • 85.
     AGE–RAGE interactionresults in immobilization of monocytes at the local site.  induces a change in monocyte phenotype, upregulating the cell and significantlymincreasing pro-inflammatory cytokine production.  increased gingival crevicularfluid production oftumor necrosis factor-a, prostaglandin E2 and interleukin-1b 159
  • 86.
     This interactionalso increases oxidant stress within the tissue, resulting in tissue destruction (166).  blocking the receptor RAGE decreases levels of the pro-inflammatory cytokines tumor necrosis factor- a and IL-6 in gingival tissues, decreases levels of tissue-destructive matrix metalloproteinases, lowers AGE accumulation in periodontal tissues and decreases alveolar bone loss in response to P. gingivalis (89).
  • 87.
  • 88.
    2- WAY RELATIONSHIPBETWEEN PERIODONTAL DISEASE AND DM
  • 89.
    EFFECT OF DIABETESON 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
  • 90.
    AUTHOR YEAR STUDY Cianciola et al 1982In children with type 1 diabetes, the prevalence of gingivitis was greater than in non-diabetic children with similar plaque levels. Sastrowijo t o S et al 1990 Improvement in glycemic control may be associated with decreased gingival inflammation. Papapano u 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 nondiabetic 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.
  • 91.
    EFFECT OF PERIODONTITISON DM  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.
  • 92.
    AUTHOR YEAR STUDY Williams RCJr., 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 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 & root planing alone compared to diabetic subjects treated with SRP plus systemic amoxicillin/clavulanic acid. Promsudt hi A et al 2005 In older, poorly controlled type 2 diabetic subjects who received SRP plus adjunctive doxycycline showed a significant improvement in periodontal health but only a non significant reduction in HbA1c values.
  • 93.
    MECHANISM BY WHICHPERIODONTAL DISEASE MAY INFLUENCE DIABETES 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
  • 94.
    EFFECTS OF DIABETESON 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.  longitudinal studies of various periodontal treatment modalities are needed to determine the healing response in individuals with diabetes compared to individuals without diabetes. Grossi SG,1996
  • 95.
    MANAGEMENT OF DIABETES 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
  • 96.
  • 97.
    ANTI AGE THERAPY 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.
  • 98.
    DENTAL THERAPY CONDIDERATION Patients with well-controlled diabetes can 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.
  • 99.
    TIMING OF TREATEMENT Patients with well controlled DM can be treated similarly to non-diabetic patients for most routine dental needs.  Keep appointments short, atraumatic, and stressfree  morning appointments  Use appropriate vasoconstrictor agents  For stressful procedures the usual drug regime may be altered
  • 100.
    Response to periodontaltreatment in patients with diabetes  Well controlled diabetes mellitus subjects with moderate to advancedmperiodontal disease, scaling and root planing resulted in similar clinical changes when compared to non-diabetes mellitus subjects 25  Conversely, poorly controlled diabetes mellitus patients often have a less favorable response to treatment
  • 101.
     initial responseto scaling and root planing was good , but the incidence of disease recurrence over the subsequent 12 months was greater in poorly controlled diabetes mellitus Individuals Tervonen et al. (188)  At the 5-year re-evaluation, diabetes mellitus patients had a similar percentage of sites gaining or losing attachment, and a similar percentage of sites with stable attachment levels, compared to non- diabetes mellitus subjects
  • 102.
    USE OF ANTIBIOTIC 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.
  • 103.
    IMPLANT PLACEMENT CONSIDERATION 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
  • 104.
     Possible DiabeticDisturbances in Implant Wound Healing Process In Implants
  • 105.
    DIABETIC EMERGENCY  Hypoglycemiccrisis  Hyperglycemic crisis
  • 106.
    HYPOGLYCEMIC CRISIS  INSULINSHOCK  Blood glucose level <60 mg/dl  Signs: sweating , tremor, dizziness, headache, loss of consciousness  Treatment : 1. recognition of hypoglycemia 2. Termination of dental procedure 3. Position- upright 4. A-B-C 5. D-definitive care – administration of oral carbohydrate (3-4 tspn of sugar/ candy)
  • 107.
    HYPERGLYCEMIC CRISIS  Dentalpt with hyperglycemia represent ASA IV risk & shouldn’t receive any dental t/t.  In unconscious pt; 1.Terminate dental procedure 2.Position - trendenlenburg 3.A-B-C 4.D- definitive care- 5% dextrose & H2O/ NS, administration of O2
  • 108.
    SPECIFIC MANAGEMENT GUIDELINES  USEOF EPINEPHRINE  Under stressful situation production of epinephrine & cortisol increases -> increase blood glucose level -> adequate pain control & stress reduction  Epinephrine is not contraindicated for LA
  • 109.
    PERIODONTAL MANAGEMENT  Periodontalt/t must be conducted in parallel with DM t/t. Taylor GW,1999  Primary t/t should be nonsurgical  Surgical t/t should be done in well glycemic controlled (100-200 mg/dl) pt , medication should be modified, it can result in prologed healing. Kripal K,2017
  • 110.
     Combination ofnonsurgical debridement & systemic antibiotic has shown better result in advance periodontitis cases Mealey BL, 2006  Combination of tetracycline & doxycycline with SRP also resulted better than SRP alone , even for topical intrasulcular doxycycline also resulted better Ship JA,2003
  • 111.
     These drugsinhibit MMPs, gcf collagenase, risk of bacterial resistance, bone resorption, bone loss.  Supportive periodontal therapy should be provided at intervals of 2-3 months.
  • 112.
    GUIDENINES FOR TREATEMENT DIABETES & PERIODONTAL DISEASE: CENSUS REPORT OF THE JOINT EFP/AAP WORKSHOP ON PERIODONTITIS & SYSTEMIC DISEASES  (CHAPPLE LC,GENCO R. J PERIODONTOL 2013)
  • 113.
    GUIDELINE- A  Patientswith 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.
  • 114.
     Patients withtype 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.
  • 115.
    GUIDELINE- B  Ifperiodontitis 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
  • 116.
     Provide oralhealth 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.
  • 117.
    GUIDELINE- C  Ifyour 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.
  • 118.
    GUIDELINE- D  Peoplewith 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.
  • 119.
    CONCLUSION  Diabetes mellitushas 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.
  • 120.
     • Advancesin 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.

Editor's Notes

  • #11 Hasimoto’s thyroiditis, addition dis, vitiligo, pernicious anaemia 5-10%
  • #12 Muscle cells 95%
  • #13 1-2%
  • #14 3rd tri Prog & other hormones In placenta impairs insulin action at cellular levl
  • #26 AGEs form in diabetic and non-diabetic individuals; however, their accumulation is greatly increased in diabetic patients with sustained hyperglycemia.
  • #46 puberty, there was a general increase in gingivitis, independent of glycemia
  • #54 After 4 days of insulin therapy