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By- Krishan Gulia

INTRODUCTION HISTORY DIABETES

MELLITUS ORAL MANIFESTATIONS OF DIABETES DIABETES AND PERIODONTAL DISEASE MICROBIOLOGY PATHOGENESIS EFFECTS OF PERIODONTAL INFECTION ON GLYCEMIC CONTROL OF DIABETES DIABETES AND DENTAL IMPLANT THERAPY

PATIENT EVALUATION MANAGEMENT OF KNOWN DIABETIC PATIENTS MANAGEMENT OF UNCONTROLLED OR POORLY CONTROLLED DIABETIC PATIENTS ORAL MEDICATIONS FOR DIABETIC CONTROL MANAGEMENT OF DIABETIC EMERGENCIES SUMMARY REFERENCES

Diabetes mellitus (DM) refers to a group of common metabolic disorders that share the phenotype of hyperglycemia. Several distinct types of DM are caused by a complex interaction of genetics and environmental factors. Depending on the etiology of the DM, factors contributing to hyperglycemia include reduced insulin secretion, decreased glucose utilization, and increased glucose production. The metabolic dysregulation associated with DM causes secondary pathophysiologic changes in multiple organ systems that impose a tremendous burden on the individual with diabetes and on the health care system. In the United States, DM is the leading cause of endstage renal disease (ESRD), nontraumatic lower extremity amputations, and adult blindness. It also predisposes to cardiovascular and periodontal diseases.

Globally, as of 2010, an estimated 285 million people had diabetes, with type 2 making up about 90% of the cases.Its incidence is increasing rapidly, and by 2030, this number is estimated to almost double. Diabetes mellitus occurs throughout the world, but is more common (especially type 2) in the more developed countries. The greatest increase in prevalence is, however, expected to occur in Asia and Africa, where most patients will probably be found by 2030.The increase in incidence in developing countries follows the trend of urbanization and lifestyle changes, perhaps most importantly a "Western-style" diet. This has suggested an environmental (i.e., dietary) effect, but there is little understanding of the mechanisms at present.

India has more diabetics than any other country in the world, according to the International Diabetes Foundation,although more recent data suggest that China has even more.The disease affects more than 50 million Indians - 7.1% of the nation's adults - and kills about 1 million Indians a year.The average age on onset is 42.5 years.The high incidence is attributed to a combination of genetic susceptibility plus adoption of a high-calorie, lowactivity lifestyle by India's growing middle class.

HISTORY
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. Bennet(1994) Ervasti et al defined this as National (1985)-defined a syndrome Malins (1968)- diabetes data diabetes characterized defined group (1979) mellitus as a by diabetes as a defined hyperglycemia metabolic chronic diabetes disorder with and mellitus as a disorder of disturbances in disturbances of carbohydrate genetically and the intrinsic carbohydrate, metabolism clinically production, of fat and protein characterized heterogenous insulin leading metabolism by group of to an abnormal associated with hyperglycemia disorders that fat, absolute or and glycosuria shared glucose carbohydrate relative . intolerance in and protein deficiencies in common. metabolism . insulin action and secretion.

The

term diabetes mellitus describes a metabolic disorder of multiple etiology characterized by chronic hyperglycaemia with disturbances of carbohydrate, fat and protein metabolism resulting from defects in insulin secretion, insulin action, or both.

Type

I diabetes: Insulin dependent diabetes mellitus Type II diabetes: non- insulin dependent diabetes mellitus Gestational diabetes

Formerly called Insulin-Dependent Diabetes Mellitus and Juvenile-Onset Diabetes. In Type I Diabetes a persons body does not produce insulin or produces it in very small amounts.The symptoms usually appear suddenly during childhood, usually around the age of puberty.In type I diabetes,the immune system attacks the insulin producing cells (called "islets") in the pancreas, making this an autoimmune disease. Patients with type I diabetes present with the symptoms traditionally associated with diabetes, including polyphagia, polydipsia, polyuria, and predisposition to infection.

Formerly called Non-Insulin Dependent Diabetes Mellitus and Adult-Onset Diabetes.In Type II Diabetes, both the bodys ability to produce insulin and to use insulin may change.The pancreas may start producing only very small amounts of insulin or the cells of the body may become resistant to the action of the insulin. The symptoms usually develop gradually over several years and the person may not realize they are ill for quite a while. Those symptoms include increased infections or skin sores, slow healing of infections, tiredness, and tingling or numbness of hands or feet. There is a strong relationship between obesity and type II diabetes. Type II diabetes usually develops after age 45, but instances in younger people are increasing as obesity rates increase.

Glucose intolerance developing during pregnancy is classified as gestational diabetes.In this condition,some women experience in the second half of their pregnancy when blood sugar levels become abnormally high. The condition usually goes away after the pregnancy but in some people it does not. Insulin resistance is related to the metabolic changes of late pregnancy, and the increased insulin requirements may lead to diabetes.

GDM occurs in 7% (range 210%) of pregnancies in the United States; most women revert to normal glucose tolerance postpartum but have a substantial risk (3560%) of developing DM in the next 1020 years.

Insulin is the principal hormone that regulates uptake of glucose from the blood into most cells (primarily muscle and fat cells, but not central nervous system cells). Therefore, deficiency of insulin or the insensitivity of its receptors plays a central role in all forms of diabetes mellitus. Insulin is released into the blood by beta cells (-cells), found in the islets of Langerhans in the pancreas, in response to rising levels of blood glucose, typically after eating. Insulin is used by about two-thirds of the body's cells to absorb glucose from the blood for use as fuel, for conversion to other needed molecules, or for storage.

Insulin is also the principal control signal for conversion of glucose to glycogen for internal storage in liver and muscle cells. Lowered glucose levels result both in the reduced release of insulin from the -cells and in the reverse conversion of glycogen to glucose when glucose levels fall. This is mainly controlled by the hormone glucagon, which acts in the opposite manner to insulin. Glucose thus forcibly produced from internal liver cell stores (as glycogen) re-enters the bloodstream; muscle cells lack the necessary export mechanism. Normally, liver cells do this when the level of insulin is low (which normally correlates with low levels of blood glucose).

Higher insulin levels increase some anabolic processes, such as cell growth and duplication, protein synthesis, and fat storage. Insulin (or its lack) is the principal signal in converting many of the bidirectional processes of metabolism from a catabolic to an anabolic direction, and vice versa. In particular, a low insulin level is the trigger for entering or leaving ketosis (the fat-burning metabolic phase). If the amount of insulin available is insufficient, if cells respond poorly to the effects of insulin (insulin insensitivity or resistance), or if the insulin itself is defective, then glucose will not have its usual effect, so it will not be absorbed properly by those body cells that require it, nor will it be stored appropriately in the liver and muscles. The net effect is persistent high levels of blood glucose, poor protein synthesis, and other metabolic derangements, such as acidosis.

1.Diabetic

Ketoacidosis 2.Hyperglycemic Hyperosmolar State 3.Hypoglycemia 4.Diabetic Nephropathy 5.Diabetic Retinopathy 6.Diabetic Neuropathy 7.High Blood Pressure 8.Slow Healing

Xerostomia and parotid gland enlargement (Sreebny LM et al.1992)

burning mouth syndrome


Altered taste sensation

Candidiasis (Fisher BM, 1987)

increased caries rate

Oral lichen planus (Bagan-Sebastian JV,1992) Alterations in the flora of the oral cavity with greater predominance of Candida albicans, hemolytic Streptococci and Staphylococci.

increased gingival inflammation in response to bacterial plaque. (Cianciola LJ et al.1982, De Pommereau V et al.1992)

Pronounced gingival enlargement.

Goldman and Cohen in (1973) - Granular subgingival proliferations

Periodontitis

Multiple lateral periodontal abscesses

Sessile or pedunculated gingival polyps

undiagnosed or poorly controlled diabetes mellitus


multiple or recurrent periodontal abscesses unexplained edematous gingival enlargement
rapid destruction of alveolar bone delayed healing

The glucose content of gingival fluid and blood is higher in individuals with diabetes than without, with similar Plaque and Gingival Index scores. Ficara AI, Levin MP in 1975 found that the increased glucose in the gingival fluid and blood of individuals with diabetes could change the environment of the microflora, inducing qualitative changes in bacteria that could account for the severity of periodontal disease observed in poorly controlled individuals with diabetes. Patients with type 1 diabetes with periodontitis have been reported to have a subgingival flora composed mainly of Capnocytophaga, anaerobic vibrios, and Actinomyces species. Porphyromonas gingivalis, Prevotella intennedia, and Actinobacillus actinomycetemcomitans, which arecommon in periodontal lesions of individuals without diabetes, are present in low numbers in those with the disease .

Gusberti F, Grossman N, Loesche in 1982 and Shklar G et al in 1962 however, found scarce Capnocytophaga and abundant A. actinomycetemcomitans and black-pigmented Bacteroides, as well as P. intermedia, P. melaninogenica, and Campylobacter rectus. Mascola B in 1970 and Sastrowijoto SH et al in 1989 found blackpigmented species, especially P. gingivalis, P. intermedia, and C. rectus, are prominent in severe periodontal lesions of Pima Indians with type 2 diabetes .These results point to an altered flora in the periodontal pockets of patients with diabetes.

Increased collagenase activity and decreased collagen synthesis is found in individuals with diabetes with chronic hyperglycemia. Decreased collagen synthesis, osteoporosis, and reduction in the height of alveolar bone occur in diabetic animals, with comparable osteoporosis in other bones. The periodontal ligament and cementum are not affected, but glycogen is depleted in the gingiva. Bissada NF in 1966 found ,generalized osteoporosis, resorption of the alveolar crest, and gingival inflammation and periodontal pocket formation associated with calculus have been described in Chinese hamsters with hereditary diabetes under insulin replacement therapy.

Chronic hyperglycemia adversely affects the synthesis, maturation, and maintenance of collagen and extracellular matrix. In the hyperglycemic state, numerous proteins and matrix molecules undergo a nonenzymatic glycosylation, resulting in advanced glycation end products (AGES). The formation of AGES can occur at normal glucose levels, but in hyperglycemic environments, AGE formation is excessive. AGE formation cross-links 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.

Periodontitis has been referred to as the sixth complication of diabetes(Loe. H, 1993) . A number of studies found a higher prevalence of periodontal disease among diabetic patients than among healthy controls. Available data reveals strong evidence that diabetes is a risk factor for gingivitis and periodontitis, and the level of glycemic control appears to be an important determinant in this relationship.( Papapanou PN in 1996)

Although Sbordone L et al in 1998 ,have not found a significant association between diabetes and gingival inflammation. Cianciola L et al in 1982 repoted that children with type 1 diabetes,and the prevalence of gingivitis was greater than in nondiabetic children with similar plaque levels. The relationship between type 2 diabetes and periodontal disease is complicated by the fact that diabetes onset generally occurs after the age of 40 years, coinciding with the time point when periodontal disease becomes more prevalent (Salvi et al. 2008) . Further evidence of type 2 diabetes as a risk factor for more severe periodontal disease has been reported by (Tsai et al. 2002; Sandberg et al. 2000; Campus et al. 2005; Jansson et al. 2006).

It was suggested that periodontal destruction can start very early in life in diabetes, becomes more prominent as children become adolescents (Lalla et al. 2006), and is related to the level of metabolic control (Lalla et al. 2007).

In adults with type 1 diabetes, the overall degree of gingival inflammation was similar between diabetic subjects as a whole and non-diabetic control subjects with similar plaque accumulation(Sastrowijoto S in 1990 and Karjalainen K in 1996).

Ervasti T et al in 1985, found greater gingival inflammation was also seen in adults with type 2 diabetes than in non-diabetic controls, with the highest level of inflammation in subjects with poor glycemic control.

Cutler CW et al in 1999 ,showed more 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.

In a large cross-sectional study, by Grossi et al in 1994 showed that diabetic patients were twice as likely as nondiabetic subjects to have attachment loss. Firatli E et al in 1997 followed type 1 diabetic patients and healthy controls for 5 years and found that the people with diabetes had significantly more clinical attachment loss than controls.

Bridges RB et al in 1996 in his cross sectional study concluded that diabetes affected all periodontal parameters, including bleeding scores, probing depths, loss of attachment and missing teeth.
A study by Moore PA et al in 1999 has shown that diabetic patients are 5 times more likely to be partially edentulous than nondiabetic subjects.

A study by Weyant RJ et al in 1998 showed that people with type I and type 2 diabetes appear equally susceptible to periodontal disease and tooth loss. Chen I and Skrepcinski FB et al in 2000 found ,a relationship between diabetes and periodontal disease,which appears to be very strong within certain populations, such as Aboriginal peoples ,which indicates a genetic component.

Myers DE et al in 1999 in his study found that ,smoking increases the risk of periodontal disease by nearly 10 times in diabetic patients.

In subjects with diabetes, chronically elevated blood glucose levels lead to the accelerated formation of advanced glycation end products (AGEs). Endothelial cells and monocytes possess specific receptors for AGEs (i.e., RAGEs) located on their cell surfaces.

There is strong indication that the interaction of AGEs with their receptors plays an important role in the development of diabetic complications. The interaction of macrophages with AGEs has been shown to stimulate increased secretions of pro-inflammatory mediators such as tumour necrosis factor a (TNF-a) and interleukin-1 (IL-1). In subjects with type 2 diabetes, deterioration of periodontal status was associated with elevated serum levels of AGEs (Salvi et al. 2008).

The possible role of adipokines in periodontal disease and type 2 DM because these mediators may reflect common pathogenic processes relating to imunoregulatory changes (Preshaw et al. 2007 and Lalla et al. 2001).

Other mechanisms by which diabetes may influence the periodontium includes: vascular abnormalities, nonenzymatic glycosylation, imbalances in lipid metabolism, altered collagen metabolism, neutrofil dysfunction and altered monocytic response (Mealey and Oates 2006 and Ryan et al. 2003)

Diabetes
Diabetic people are 2-4 times more susceptible to periodontal disease

Periodontal Disease

Periodontal infection then complicates glycemic control and enhances insulin resistance and hyperglycemia

Poor glycemic control causes increased susceptibility to re-infection and more severe periodontal disease

Well controlled Diabetes mellitus subjects with moderate to advanced periodontal disease, scaling and root planing resulted in similar clinical changes when compared to nondiabetes mellitus subjects with similar levels of periodontal disease.(Christgau et al.in 1998)

Conversely, poorly controlled diabetes mellitus patients often have a less favorable response to treatment than those with well controlled diabetes.
Tervonen et al in 1997 ,found that the initial response to scaling and root planing was good in diabetes mellitus subjects, but the incidence of disease recurrence over the subsequent 12 months was greater in poorly controlled diabetes mellitus individuals compared to well or moderately controlled subjects.

Westfelt et al in 1996, performed a longitudinal assessment of periodontal therapy, including scaling and root planing, modified Widman flap surgery, and regular maintenance, in diabetes mellitus subjects and non-diabetes mellitus controls with moderate to advanced periodontitis. At the 5-year reevaluation, 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 nondiabetes mellitus subjects. This data suggest that individuals with well controlled diabetes mellitus respond to periodontal therapy in a fashion similar to non-diabetes mellitus patients, but that poorly controlled patients may have a less favorable response.

There is little scientific evidence regarding the success or failure of dental implant therapy in diabetic individuals. Diabetes is often considered a relative contraindication to implant placement, but in well-controlled diabetes there is no reason to avoid implant therapy. Patients with poorly controlled diabetes may not respond well to any surgical treatment, including implant placement, due to impaired wound healing. The effect of diabetes on long- term clinical implant stability is also unknown at this time.

Surgical implant osteotomy

Possible diabetic disturbances in the implant wound-healing process


Changes in wound healing proteins

Blood clot formation Bone resorption phase Matrix formation phase Bone deposition/osteoid mineralization Maintenance of osseointegration

Decreased number of osteoclasts

Inhibition of collagen formation


Decreased number of osteoblasts Mineralization proteins reduced
Reduced bone turnover Alterations in bone homeostasis Change in diabetic status

Pinche

JE 1998- (hemoglobin A1c)


one medical laboratory test and patient compliance is not required

measures blood glucose levels over a period of 8 to 12 weeks.

accurate and relatively inexpensive

Long term glycemic control

Provide an indication of potential response to periodontal therapy

4%-6% < 7% 7%-8% >8%

Normal Good diabetes control Moderate diabetes control Action suggested to improve diabetes control

Home

monitoring devices test their blood glucose levels four to six times daily.

one or two-drop blood sample simple,

reagent reflector strip monitor inexpensive and

reasonably accurate used in dental offices as a screening test

Primary treatment goals for DM are achieving blood glucose levels that are as close to normal as possible and prevention of diabetic complications.Other goals are normal growth and development, normal body weight, the avoidance of sustained hyperglycemia or symptomatic hypoglycemia, the prevention of diabetic ketoacidosis and nonketotic acidosis, and the immediate detection and treatment of long-term diabetic complications. Diet, exercise, weight control, and medications are the mainstays of diabetic care. Obesity is very common in type 2 DM and contributes greatly to insulin resistance. Weight reduction and exercise improve tissue sensitivity to insulin and allow its proper use by target tissues.

Sulfonylureas stimulate pancreatic insulin secretion. The increased quantity of secreted insulin helps counteract the qualitative decrease in tissue sensitivity to insulin, allowing greater glucose entry into target cells and thereby lowering blood glucose levels. Sulfonylureas have a relatively long duration of action (1224 hours), depending on the drug, and are taken once or twice per day. Hypoglycemia is a major side effect of sulfonylureas. In patients taking these agents, food intake must be adequate to prevent glucose levels from falling too low.

Metformin

is a biguanide agent that lowers plasma glucose mainly by preventing glycogenolysis in the liver. Metformin also improves insulin use, counteracting the insulin resistance seen with type 2 DM. Because metformin does not stimulate increased insulin secretion, hypoglycemia is much less common with this drug.

Insulin is taken via subcutaneous injection, most often with a syringe. Insulin infusion pumps deliver insulin through a subcutaneous catheter. There are a variety of insulin preparations available; they vary in their onset, peak, and duration of activity and are classified as long-, intermediate-, short-, or rapid-acting. Ultralente insulin is the longest-acting insulin. Commonly called peakless insulin, Ultralente has a very slow onset of action, minimal peak activity, and a long duration of action. The rapid-acting insulin (lispro insulin) is rapidly absorbed, becomes active about 15 minutes after injection, and is at peak activity at 30 to 90 minutes.

An emerging therapeutic option for type 1 DM is transplantation of the whole pancreas or pancreatic islet cells.Both are still complicated by major side effects and are thereby performed in patients who have already developed significant morbidity from DM. With the development of continuous glucosemonitoring technology, it may now be possible to use closed-loop pumps that infuse the correct amount of insulin in response to changing blood glucose levels.

Glycemic control plays a role in the response of DM patients to periodontal surgery. Poorly controlled diabetics are highly susceptible to dentoalveolar infections ,as they respond less favorably to both surgical and nonsurgical periodontal therapy, and short-term improvements in periodontal health are frequently followed by regression and disease recurrence. A patient presenting with signs and symptoms of undiagnosed or poorly controlled DM (see above) should be referred to a physician for diagnosis and treatment. Antibiotic prophylaxis may be indicated if a patient's HbA1c level is very high (>11 12%) and there are signs of recurrent intraoral bacterial infections

If the patient has renal insufficiency, potentially nephrotoxic drugs (eg, acetaminophen, acyclovir, aspirin, nonsteroidal antiinflammatory drugs [NSAIDs]) should be avoided or dosages revised.

Patients undergoing periodontal or oral surgery procedures other than single, simple extractions should be given dietary instructions after surgery; these instructions should be established with input from the patients physician and nutritionist Appointment scheduling is often determined by the individuals medication regimen. Traditionally, it was recommended that medically complex patients, including those with DM, receive dental treatment in the morning to reduce stress,. The greatest risk would occur in a patient who has taken the usual amount of insulin or oral hypoglycemic agent but has reduced or eliminated a meal prior to dental treatment.

For example, if the patient takes the usual dose of regular insulin before breakfast but then fails to eat or eats less than the usual amount, the patient will be at increased risk of hypoglycemia during a morning dental appointment. the best time for dental treatment is either before or after periods of peak insulin activity. This reduces the risk of perioperative hypoglycemic reactions, which occur most often during peak insulin activity

Treatment of oral fungal infections in the patient with DM is similar to standard regimens except that topical antifungal medications should be sugar free. Studies conducted by (Williams & Mahan 1960; Grossi et al. 1997; Miller et al. 1992) including antibiotics as an adjunct to mechanical therapy reported a limited, short-term improvement in metabolic control. Grossi et al. in 1997 reported a 10% improvement in glycated hemoglobin (HbA1c) at 3 months after the completion of non-surgical periodontal therapy combined with adjunctive systemic doxycycline, although this effect was not sustainable at later time points.

Whereas, Rodrigues et al in 2003 randomly assigned 30 type 2 patients to two treatment groups, one group receiving non-surgical periodontal therapy with amoxicillin/clavulanic acid and the other receiving only mechanical therapy. At 3 months, HbA1c levels were reduced in both groups, but the reduction was statistically significant only in the group that received scaling and root planing alone.