Type 1 (Insulin Deficient)

Type 1 diabetes mellitus, which involves about 5% to 10% of the diabetic population, commonly occurs in childhood and adolescence but can strike at any age. Individuals who develop type 1 diabetes mellitus are rarely obese. An absolute deficiency of insulin secretion is characteristic in this type, and treatment requires regular lifelong administration of insulin by injection to prevent ketosis and sustain health. The disease results from destruction of the beta cells of the pancreas with abrupt symptoms in children and slow onset in adults. Genetic predisposition related to the presence of certain human leukocyte antigens (HLAs) that influence immune activity directed against islet cells is essential for type 1 diabetes. Research studies suggest a genetic origin associated with type 1 and type 2 diabetes. The role of genetics is weaker in type 1 diabetes than in type 2 diabetes. Environmental factors, still poorly defined, are postulated to play a causative role in genetically predisposed individuals. Autoimmune reaction and environmental factors, such as viral infection, have been demonstrated in research. Twin studies reveal that if one twin develops type 1 diabetes, the other twin will develop the disease in approximately 50% of cases.³

Type 2 (Insulin Resistant)

Type 2 diabetes mellitus is recognized as a heterogeneous disorder that results from insulin resistance and insulin secretory defect. Most individuals with type 2 diabetes are obese, and obesity itself causes some degree of insulin resistance. Individuals who are not obese by traditional weight criteria may have an increased percentage of body fat distributed in the abdominal region. People with type 2 diabetes constitute approximately 90% to 95% of the diabetic population. Of the undiagnosed the vast majority have type 2 diabetes. Risk of developing type 2 diabetes increases with obesity, age, lack of physical activity, history of GDM, hypertension, and dyslipidemia (abnormal amounts of blood lipids). Frequency of type 2 diabetes varies with racial and ethnic groups. Ketoacidosis seldom occurs in type 2 diabetes, but when present, it is associated with infection. Type 2 diabetes usually goes undiagnosed for years because hyperglycemia develops gradually without classic symptoms. Nevertheless, risk of developing macrovascular and microvascular complications (problems in the large and small blood vessels) is high. Symptoms may be gradual, and weight loss is uncommon (Table 43-2).

TABLE 43-2 Complications of Diabetes Mellitus

Persons with type 2 diabetes often respond to weight reduction, dietary management, exercise, and oral hypoglycemic medications. Persons with type 2 diabetes may require insulin therapy to achieve good control or during illness, which is an important distinction between insulin-dependent and insulin-treated individuals.

Predominantly, type 2 diabetes is genetically inherited and has no association with autoimmune beta-cell destruction. In studies, if one twin develops type 2 diabetes the other twin has a 100% chance of developing the disease.³ Obesity has a major role in the development of type 2 diabetes, but more research is needed.

Gestational Diabetes Mellitus

Gestational diabetes mellitus occurs in 4% of pregnancies in the United States⁴ and represents 90% of all pregnancies complicated by diabetes. Clinical characteristics include glucose intolerance that has its onset or recognition during pregnancy. Therefore diabetic women who become pregnant are not in the GDM classification. High-risk individuals include women with the following conditions:

Marked obesity

Previous GDM

Strong family history of diabetes

Glucosuria (glucose in urine)

Even in the nondiabetic individual, normal pregnancy affects both fetal and maternal metabolism and exerts a diabetogenic effect. GDM generally reverts following birth because the condition is a consequence of the normal anti-insulin effects of pregnancy hormones and diversion of natural glucose to the fetus.

GDM increases risk of perinatal morbidity and mortality. Maternal complications include increased rate of cesarean delivery and chronic hypertension. Furthermore, women with a history of GDM are at increased risk for developing diabetes 5 to 10 years later. Six weeks or more after pregnancy ends, the woman with GDM should be reclassified as having one of the following:

Diabetes

Impaired glucose tolerance (IGT) or normoglycemia

Impaired fasting glucose

Other Specific Types of Diabetes Mellitus

The category of other specific types of diabetes mellitus is heterogeneous in nature and includes diabetes in which the causative relationship is known, such as diabetes mellitus associated with certain conditions and syndromes (e.g., genetic defects of the beta cells, pancreatic disease, endocrine disease, chemical-induced agents, and genetic syndromes). In other diabetic disorders such as genetic syndromes associated with glucose intolerance, a causative relationship is suspected. Rare and highly specific causes of diabetes and insulin resistance include defects in insulin receptors located on the cell membrane and conditions such as systemic lupus erythematosus in which insulin-receptor antibodies may develop. In addition to the presence of the specific condition or syndrome, diabetes mellitus also is present.

Prediabetes

The designations impaired glucose tolerance and impaired fasting glucose (IFG) are metabolic stages intermediate between normal glucose homeostasis and diabetes. IGT and IFG have been officially termed prediabetes and designated as risk factors for future diabetes and cardiovascular disease (CVD). Individuals at high risk for developing diabetes can be given a wide variety of interventions that can delay, and sometimes prevent diabetes onset. IGT can be determined only by an oral glucose tolerance test (OGTT) consisting of a standard glucose challenge followed 2 hours later by measurement of venous plasma glucose concentration. IFG is determined by a fasting plasma glucose test. Disease management includes dietary control of obesity, treatment of hypertension and hyperlipidemia (high amounts of fat in the blood), and elimination of smoking, if the individual smokes (Figure 43-1 and see Box 43-2).

Figure 43-1 Prediabetes glucose levels.

(With permission from Fehrenbach MJ: Dental care for the diabetic patient, Prev Angle Newsl 4:1, 2005.)

Insulin Deprivation

The net effect of insulin deficiency is that blood glucose concentration rises (hyperglycemia). Without insulin, the glucose derived from a meal cannot be used or stored. When the blood glucose level rises >150 mg/dL, the kidney tubules become incapable of resorption. Glucose appears in the urine (glucosuria), taking with it a large amount of fluid, thus raising the volume of urine (polyuria) and necessitating frequent urination. Dehydration follows, leading to excessive thirst (polydipsia). Ketoacidosis may follow hyperglycemia when blood glucose levels rise to >400 mg/dL (Box 43-3). Impaired carbohydrate metabolism, which the body interprets as energy starvation, causes excessive ingestion of food (polyphagia) and necessitates use of fats and proteins (hyperglycemia progressively glycates body proteins) to satisfy energy requirements. Ketoacids and ketone bodies (acetone) are produced as a result of catabolism of fatty acids (lipolysis). Ketones accumulate in the tissues, are excreted in the urine (ketonuria), and circulate in the blood (ketonemia), causing a drop in the pH of the blood and leading to diabetic coma.

Clinical Signs and Symptoms

Diabetes is characterized by hyperglycemia. In type 1 diabetes mellitus, the predominant problem is impaired insulin production, whereas in type 2 diabetes mellitus the predominant problem is the inability to use the insulin produced by the body. A considerable overlap exists, however, in clinical features of the two forms of diabetes. The deficiency of insulin action leads to derangements of the intermediary metabolism of carbohydrates, protein, and lipids. In clinical practice the suspicion of diabetes is gleaned from history and physical findings (Box 43-4).

Indicators of probable diabetes mellitus (cardinal signs of diabetes) are as follows:

Polydipsia

Polyuria

Polyphagia

Unexplained weight loss

Weakness

Symptoms of marked hyperglycemia also include polyphagia (eating extreme amounts of food) and blurred vision. Impairment of growth and susceptibility to certain infections may also accompany chronic hyperglycemia. A family history of diabetes, obesity, GDM, premature atherosclerosis, and neuropathic disorders also are indications of probable diabetes mellitus (Boxes 43-5, 43-6, and 43-7).

Chronic Complications

People with both types of diabetes mellitus show a tendency for severe, multisystem, long-term complications (see Table 43-2), including the following:

Microvascular and macrovascular disease

Diabetic retinopathy with potential loss of vision

Nephropathy leading to renal failure

Peripheral neuropathy with risk of foot ulcers, amputation, and neuropathic joint disease

Autonomic neuropathy causing gastrointestinal, genitourinary, and cardiovascular symptoms and sexual dysfunction

Periodontal disease

Mechanisms thought to cause tissue damage in diabetics are alterations in the host immunoinflammatory response including altered function of immune cells (including neutrophils, monocytes, and macrophages), elevated levels of tumor necrosis factor-alpha (TNF-α), alterations in connective tissue metabolism, glycation of tissue proteins forming advanced glycation end products (AGEs)⁵ and AGE-modified collagen.⁵ Individuals with diabetes have an increased incidence of atherosclerotic, cardiovascular, peripheral vascular, and cerebrovascular disease. Hypertension, abnormalities in lipoprotein metabolism, and periodontal disease are found in people with diabetes. The emotional and social impact of diabetes and the demands of therapy cause significant unmet human needs in individuals with diabetes and their families (Table 43-3). All complications affect clients with both type 1 and type 2 diabetes, although clinical consequences differ greatly. Generally, kidney and eye diseases predominate in type 1 diabetes, atherosclerotic disease predominates in type 2 disease, and neuropathy occurs in both (see Table 43-2).

TABLE 43-3 Some Unmet Human Needs of Persons with Diabetes and the Effect on Outcomes of Self-Monitoring of Blood Glucose

Adapted from Skyler JS, Reeves ML: Intensive treatment of type I diabetes mellitus. In Olefsky JM, Sherwin RS, eds: Diabetes mellitus: management and complications, New York, 1985, Churchill Livingstone.

Diabetes—A Risk Factor for Periodontal Disease

See Chapter 17, section on modifiable risk factors, and Chapter 18.

Periodontal disease is the sixth complication of diabetes. Young adults with diabetes have twice the periodontal disease risk of those without diabetes. One third of individuals with diabetes have severe periodontal disease with attachment loss of 5 mm or greater.⁶ Level of glycemic control seems to be an important determinant in the relationship.

Hypoglycemia (see Box 43-7; Tables 43-4 and 43-5)

Hypoglycemia (blood glucose concentration <50 mg/dL), the most common metabolic emergency in persons with type 1 diabetes mellitus, is a condition resulting from an excess of insulin and a glucose deficiency in the body. (Blood glucose concentration of 80 to 120 mg/dL is normal). Annually, severe episodes occur in one of five individuals; minor episodes occur every 2 weeks on average in each insulin-treated person. In clients with type 2 disease treated with sulfonylurea agents, hypoglycemia is more common than is generally recognized and may be severe, especially in older persons treated with longer-acting agents. Signs and symptoms of hypoglycemia result from a lack of glucose in the brain and compensation by the nervous system for this lack of glucose (see Box 43-7). Main causes of hypoglycemia in persons with type 1 disease are listed in Table 43-4.

TABLE 43-4 Causes of Hypoglycemia in Type 1 Diabetes Mellitus

TABLE 43-5 Hypoglycemia Compared with Hyperglycemia

Individuals with diabetes can manage mild hypoglycemia themselves by ingesting glucose, sweet drinks, or milk. Between 10 and 20 g of glucose (about the amount in an 8-ounce glass of 2% fat milk, a 4-ounce glass of orange juice, three pieces of hard candy, or eight Lifesavers candies) is generally adequate, although many persons take considerably more because they fear prolonged hypoglycemia. More severe hypoglycemia also can be treated by oral ingestion of carbohydrates, but another person may have to administer it. If the victim is unconscious, treatment requires intravenous dextrose solution or an intramuscular injection of 0.5 mg to 1.0 mg glucagon, followed on awakening by oral complex carbohydrate with a protein source (e.g., small meat or cheese sandwich or cottage cheese and fruit).

Hyperglycemic Ketoacidotic Coma (Diabetic Coma) (see Table 43-5)

Although the percentage of all diabetic deaths caused by hyperglycemia ketoacidotic coma has decreased dramatically from more than 60% in preinsulin days to 1% at present, it is still considerable, especially in younger individuals. Prevention is the best treatment; however, emergency treatment requires hospitalization to correct fluid and electrolyte imbalances.

Coma resulting from absolute insulin deficiency is found in persons with acute-onset type 1 diabetes in whom diagnosis was unknown or delayed and in individuals with known diabetes who discontinued or decreased their insulin dose for some reason. Coma from a temporary insulin deficiency may be caused by infection or stressful situations in which there is an increase in secretion of anti-insulin hormones (glucagon, cortisol, and catecholamines) (Box 43-8). Infection is the most common precipitating factor and is present in more than 50% of all persons with diabetic ketoacidotic coma.

A series of biochemical events explains the basis of severe ketoacidosis, and signs and symptoms are presented in Table 43-6. Clear guidelines on maintaining control should be provided to the diabetic client with intercurrent infection to resolve the infection early (Box 43-9).

TABLE 43-6 Features of Severe Diabetic Ketoacidosis

∗ Indicates speculated or unknown cause.

Treatment of diabetic ketoacidosis requires hospitalization to restore the disturbed metabolic fluid and electrolyte state to normal. Fluid rehydration (salt and water), insulin, potassium, broad-spectrum antibiotic therapy, and treatment of precipitating factors are the main elements of diabetic coma treatment.

Glycemic Control: Self-Monitoring of Blood Glucose and A_1c

The most important clinical advance in the control of diabetes mellitus is self-monitoring of blood glucose with small, automated devices. Blood glucose levels can be monitored as needed; however, four times per day is generally recommended. Monitoring is done by placing a small drop of blood on a reagent strip, which is then inserted into the meter. The meter measures glucose concentration and displays a value of glucose in millimeters per deciliter (mm/dL) of blood.

The hemoglobin A_1c laboratory test (also known as the A_1c test) is used by the physician to monitor overall glycemic control. Hemoglobin A is made during the 120-day life span of a red blood cell. Blood glucose attaches to the hemoglobin A and is used as a record of blood glucose levels over the past 3 to 4 months. The normal A_1c level is <6%.² Abnormal A_1c levels correlate with glucose intolerance and the development of diabetic complications. Recommendations for A_1c levels and blood measurements are presented in Box 43-10.

Medical Nutrition Therapy

Diet remains the hallmark of diabetes therapy, despite advances in insulin formulations, insulin delivery systems, and oral medications. Diabetic diets are designed to provide appropriate quantities of food at regular intervals, supply daily caloric requirements to aid in achieving or maintaining desirable body weight, and reduce fat intake to correct an unfavorable lipid profile conducive to atherosclerosis.

In type 2 diabetes, reduction in hyperglycemia is correlated with weight loss. In type 1 diabetes mellitus, nutritional strategies involve monitoring the percentage of carbohydrate (55% to 60% of total calories) to protein (12% to 20% of total calories) intake. Meal planning for diabetics is based on the food exchange list system of the American Diabetes Association.

Insulin Therapy

Persons with type 1 diabetes have essentially no pancreatic insulin, are unresponsive to oral sulfonylurea hypoglycemic agents, and are ketosis-prone; they are therefore dependent on lifelong administration of exogenous insulin. Approximately 40% of people with type 2 diabetes use insulin to control hyperglycemia, 49% use oral medications, and 10% use a combination of insulin and oral medications.

Human insulin and insulin analogues are categorized by speed of onset, peak effect, and time of action as follows:

Rapid-acting

Short-acting

Intermediate

Long-acting

Insulin may be injected subcutaneously with an insulin syringe or a penlike device. Insulin pumps are widely used to deliver a programmed, steady drip of insulin (basal rate) under the skin 24 hours a day. A push of a button on the pump delivers a bolus dose to respond to the number of carbohydrate grams consumed at a meal. Alternative routes of insulin delivery include inhaled insulin (Exubera) and implantable insulin pumps, used in Europe. Exubera is a powdered form of insulin inhaled into the lungs through the patient's mouth using a specially designed inhaler. Table 43-7 illustrates insulin types that may be used alone or in combination. Dosages, frequency, and times of administration are highly individualized.

TABLE 43-7 Types of Insulin Preparations

Oral Drug Therapy

When type 2 control of hyperglycemia is not achieved with diet and exercise, oral drug therapy is prescribed by the physician (endocrinologist). Generally, oral drug therapy stimulates the pancreas to secrete more insulin, increases the body's response to insulin, slows digestion, or decreases glucose production, as follows:

Sulfonylureas (glyburide [Glynase Pres Tab, Micronasc], glipizide [Glucotrol]) stimulate the pancreas to increase insulin production and with the extended-release formulas have low risk of weight gain and hypoglycemia.

Metformin (Glucophage) decreases the amount of glucose secreted by the liver. Hypoglycemia is not a side effect, but this medication usually decreases appetite. Metformin is contraindicated with several other medications commonly prescribed for diabetic conditions.

Alpha-glucosidase inhibitors (AGIs) (acarbose [Precose], miglitol [Glyset]) inhibit enzymes in the small intestines, which are responsible for the digestion of starchy food, thus delaying carbohydrate metabolism.

Thiazolidinedione (Actos, Avandia) make the body more sensitive to insulin. Target cell response to insulin is improved, thus reducing insulin doses. Used for individuals with type 2 diabetes treated with insulin whose hyperglycemia is not adequately controlled. Sometimes referred to as “insulin reducers.”

Meglitinides (repaglinide [Prandin], nateglinide [Starlix]) increase insulin secretion in the presence of glucose. These drugs are prescribed for persons taking Glucophage who still do not have good diabetic control.

Injectable Agents for Type 2 Diabetes

The following are injectable agents for type 2 diabetes:

Exenatide (Byetta), derived from the saliva of the Gila monster, stimulates the incretin effect (increased insulin response), which is diminished in type 2 diabetics.

Amylinomimetics are an analog of human amylin, which modulates gastric emptying.

Assessment

Health History

In taking the health history the dental hygienist questions the client regarding the signs and symptoms of ketoacidosis (see Box 43-3) to determine whether an undiagnosed diabetic condition is present.⁷ High-risk factors for developing diabetes include the following:

Over 45 years of age (incidence of diabetes increases with age)

Diabetic family members (parent, brother, or sister)

Seriously overweight for age group

Women who have had high-birthweight babies (≥9 pounds)

Little or no daily exercise

African American, Hispanic American, Pacific Islander, or Native American ethnicity

IGT

An expanding waistline, elevated levels of triglycerides, and tendency toward hypertension

Among the aging, classic symptoms do not usually manifest. Rather, clinical findings are related to chronic complications of the disease, such as vascular disorders or neuropathic syndromes.

If the person is a known diabetic, the client and health history interview should address the following:

Date of onset of diabetes

Type of diabetes

Regularity of appointments with a physician

Methods for controlling diabetes (medications, diet, exercise, weight loss)

Date of last insulin reaction

Frequency of self-monitoring of blood glucose

Results of self-monitoring (trends and day of appointment)

Fasting blood glucose levels

Blood glucose levels 2 hours after meals

Date and results of last A_1c test

Medication schedule and dosages

Six complications of diabetes

The decision to continue the assessment, consult with a physician, or defer treatment and refer to the physician should be made based on client response to questions during health history and pharmacologic assessment (Boxes 43-11, 43-12, and 43-13).

BOX 43-11 Levels of Blood Glucose for Care Planning

With permission from Fehrenbach MJ: Dental care for the diabetic patient, Prev Angle Newsl 4:1, 2005.

• <70 mg/dL: Too low; tendency toward hypoglycemia. Provide 15 mg of carbohydrates and wait 15 minutes. If condition continues, check with a physician. Risk for emergency situations.^∗

• 80-150 mg/dL: Normal levels.

• 150-240 mg/dL: Higher levels. Monitor infections, insulin intake, stress, food intake.

• >240 mg/dL: Too high; tendency toward hyperglycemia. Check with physician. Risk for emergency situations.^∗

^∗ Indicates dental hygiene care should not be provided at this blood glucose level.

BOX 43-12 When to Refer to a Physician

Adapted from Little JW, Falace DA: Dental management of the medically compromised patient, ed 7, St Louis, 2007, Mosby.

Refer client to physician for diagnosis and/or treatment when client has the following:

• Cardinal signs of diabetes (see Box 43-3)

• Symptoms that suggest diabetes

• Estimated fasting blood glucose level of 126 mg/mL or higher

• 2-hour postprandial (following a meal) blood glucose level of 200 mg/mL or higher

• Long period since client was last seen by a physician

• Frequent episodes of hypoglycemia

• Diagnosed diabetes plus signs and symptoms of diabetes (not controlled)

• Type 1 diabetes with extreme hyperglycemia and hypoglycemia

• An infection (anywhere in the body)

BOX 43-13 When to Consult with Client's Physician

Adapted from Little JW, Falace DA: Dental management of the medically compromised patient, ed 7, St Louis, 2007, Mosby.

• Client has type 1 or 2 diabetes—determine level of control

• Client has complications such as renal disease or cardiovascular disease

• Client takes insulin

• Client is not under good medical management

• Client is undergoing extensive periodontal or oral-maxillofacial surgery

Oral Assessment

Intraoral findings may reveal the following conditions common in poorly controlled diabetes (Table 43-8):

Cheilosis

Xerostomia

Glossodynia

Enlarged salivary glands

Increased glucose in saliva

Fungal infections such as candidiasis (thrush)

Dental caries

Periodontal disease

TABLE 43-8 Oral Complications of Diabetes Mellitus

Clinical Signs and Symptoms	Pathophysiology
Salivary and Oral Changes
Xerostomia	Increased fluid loss
Bilateral, asymptomatic parotid gland swelling with increased salivary viscosity	Increased fatty acid deposition Increased salivary glucose levels Compensatory hypertrophy due to a decrease in saliva production
Increased dental caries, especially in cervical region	Secondary to xerostomia and salivary glucose levels
Unexplained odontalgia and percussion sensitivity (acute pulpitis)	Pulpal arteritis from microangiopathies
Lingual erosion of anterior teeth∗	Complications of anorexia nervosa and bulimia
Periodontal Changes
Periodontal disease† Tooth mobility Rapidly progressive pocket formation Gingival bleeding Subgingival polyps	Induction and accumulation of AGEs Degenerative vascular changes Microangiopathies Local factors Cause unknown
Infection and Wound Healing
Slow wound healing (including periapical lesions after endodontics) and increased susceptibility to infection Oral ulcers refractory to therapy, especially in association with a prosthesis Irritation fibromas Increased incidence and prolonged healing of dry socket	Hyperglycemia reduces phagocytic activity Ketoacidosis may delay chemotaxis of granulocytes Vascular changes lead to decreased blood flow Abnormal collagen production Microangiopathies Neuropathies Altered wound healing Degenerative vascular changes Postextraction infection
Tongue Changes
Glossodynia Median rhomboid glossitis (glossal central papillary atrophy)	Neuropathic complications Xerostomia Candidiasis Candida albicans
Other Changes
Opportunistic infections: Candida albicans and mucormycosis Acetone or diabetic breath (seen when the person is close to a diabetic coma) Increased incidence of lichen planus (as high as 30%)	Repeated use of antibiotics Compromised immune system Ketoacidotic state Compromised immune system

AGE, Advanced glycation end product.

∗ Although not a complication of diabetes per se, this pattern is seen when the person wants to maintain the weight-loss aspect of diabetes while ignoring or tolerating the hyperglycemic side effects. Client may not be taking proper insulin doses and may not be truthful when asked about this.

† Periodontal disease is seen in up to 40% of diabetic patients. Adequate periodontal therapy may result in decreased insulin requirements.

Adapted from Lalla RV, D'Ambrosio JA: Dental management considerations for the patient with diabetes mellitus, J Am Dent Assoc 132:1425, 2001.

Diabetes is an important risk factor for periodontal disease. The American Academy of Periodontology published a comprehensive review on diabetes mellitus and periodontal disease.⁵ Prevalence and severity of periodontal disease increase in individuals with both type 1 (insulin deficient) and type 2 (insulin resistant) forms of diabetes, as compared with nondiabetics. Diabetics with blood glycated hemoglobin A_1c levels >8% have a greater increase in periodontal inflammation, attachment loss, and bone loss than diabetics with A_1c levels <8%.⁸ Presence of hyperglycemia contributes to enhanced periodontal inflammation and alveolar bone loss in diabetes. Hyperglycemia progressively leads to an increase of proinflammatory cytokines such as TNF-α, interleukin 6 (IL-6), and others that destroy the connective tissue and bone. The chronic increased cytokine levels augment inflammatory tissue destruction. Control of hyperglycemia reduces the level of proinflammatory cytokines. Glycemic control is an integral part of the control of periodontal disease in individuals with diabetes (see Figure 43-2).⁵

Uncontrolled diabetes increases dental caries risk as a result of reduced saliva secretion and increased glucose in saliva. Other oral complications associated with diabetes may affect nutrition by causing the person to select foods that are easy to chew but nutritionally inadequate.

Diagnosis and Planning

A dental hygiene care plan focuses on the client's unmet human needs and allows the clinician to manage risks of potential diabetic emergencies, thereby protecting the client from health risks. Persons with diabetes may not be under good glycemic control. In a study of 97 patients who entered a dental clinic, 28 patients were found to be hyperglycemic (>130 mg/100 mL) and 2 were noted to be hypoglycemic (<70 mg/100 mL)⁹ (see Box 43-11). Appointments should be brief to minimize anxiety and stress and avoid interference with medication and eating schedule. Morning appointments are ideal because most people with diabetes are best controlled at this time. An hour to an hour and a half after breakfast is best for appointments to avoid the peak action time of medication. Regular (fast-acting) insulin, often taken in the morning or at each meal, peaks within 2 to 3 hours after the injection. Oral hypoglycemic agents do not cause peaks.

Therapeutic scaling and periodontal debridement are contraindicated for people in the uncontrolled diabetic condition (blood glucose levels <70 mg/dL and >240 mg/dL) (see Box 43-11and Figure 43-3). Clients should be treated in consultation and referred to the physician of record for systemic evaluation. Dental hygiene care should not begin until the diabetic condition is controlled. The short-term risk for infections in persons with diabetes has been shown to increase with average blood glucose levels of 200 to 230 mg/100 mL.³ When care is planned, interventions are likely to include the following:

Emphasis on oral biofilm control

Health status monitoring

Nutritional and dietary analysis (see Chapter 33)

Fluoride and chlorhexidine therapies and use of xylitol-containing and amorphous calcium phosphate – containing products (see Chapter 31)

Salivary replacement therapy

Systemic doxycycline therapy prescribed by dentist⁵ (see Chapter 29)

Frequent periodontal maintenance intervals¹⁰

Collaboration with physician and certified diabetes educator

A sample dental hygiene care plan is shown in the Critical Thinking Exercises section. Other management concerns are shown in Box 43-14.

Implementation

Evaluation

The periodontal tissues of the client with well-controlled diabetes respond positively to nonsurgical periodontal therapy. Delayed healing, however, may indicate hyperglycemia, which decreases the normal healing actions of leukocyte phagocytosis, chemotaxis, and adherence properties. Frequent oral assessments, periodontal maintenance, and monitoring of diabetic control with current hemoglobin A_1c test results are recommended.

CLIENT EDUCATION TIPS

Relate diabetic client's greater risk of infection and increased healing times to need for oral biofilm control.

Teach use of daily subgingival irrigation for target delivery of antimicrobial agent or twice daily use of an American Dental Association–accepted antimicrobial mouth rinse; use of an antiplaque, antigingivitis dentifrice; use of caries control products (fluoride mouth rinse, xylitol mints and chewing gum, products containing amorphous calcium phosphate [ACP]); and use of saliva replacement therapy (artificial saliva, sucking on ice chips, xylitol gum and mints).

Discuss maintenance of dentition for chewing healthy foods; diet and nutrition are essential in control of diabetes.

Emphasize that individuals with diabetes may not tolerate dentures because of oral conditions.

Stress meticulous daily oral biofilm removal as a method to control oral disease progression and diabetes. Oral health contributes significantly to long-term systemic health in the diabetic client.

LEGAL, ETHICAL, AND SAFETY ISSUES

Collaborate with the physician when healing is delayed after periodontal instrumentation.

Collaborate with the certified diabetes educator, health education consultant, or staff at hospital-based diabetes management centers.

Dental hygienists can collaborate with diabetes management centers, for example, sharing expertise in oral disease prevention, client education, oral health screenings, and referrals.

KEY CONCEPTS

Many people with diabetes do not know they have the condition.

Type 1 diabetes involves about 5% to 10% of the diabetic population. These individuals need to take insulin injections.

Presence of certain human leukocyte antigens creates a genetic predisposition for the autoimmune cause of type 1 diabetes mellitus.

Type 2 diabetes involves about 90% to 95% of the diabetic population. These individuals usually respond well to weight reduction, dietary management, exercise, or oral medications.

Insulin resistance or a defect in insulin secretion is the cause of type 2 diabetes. Risk of developing type 2 diabetes increases with obesity, age, inactivity, history of gestational diabetes mellitus (GDM), hypertension, and dyslipidemia.

GDM occurs in 4% of pregnancies. Those at high risk include women with obesity, family history of diabetes, and previous GDM.

GDM usually disappears after birth because the condition is a consequence of the normal anti-insulin effects of pregnancy hormones and the diversion of natural glucose to the fetus.

Without insulin, glucose remains in the blood (hyperglycemia) rather than being stored or used by the cells to produce energy. Suspicion of diabetes is gleaned from a history of symptoms: glucosuria, polyuria, polydipsia, weight loss, polyphagia, and blurred vision.

Diabetes mellitus causes severe multisystem, long-term complications. Kidney and eye diseases predominate in type 1 diabetes mellitus; atherosclerosis predominates in type 2; peripheral nerve disease occurs in both.

Hypoglycemia, the most common emergency in persons with type 1 diabetes mellitus, results from an excess of insulin and a deficiency of glucose.

Hyperglycemic ketoacidosis requires hospitalization to correct fluid and electrolyte imbalances.

Infection is the most common precipitating factor of hyperglycemic ketoacidosis.

Well-controlled diabetes occurs when the individual's blood glucose level is within the normal range as a result of a careful balance of medication, diet, and exercise.

Emotional stress (induced in the oral healthcare setting) causes a release of epinephrine, which mobilizes glucose in the body, contributing to a hyperglycemic condition becoming ketoacidotic.

Strict application of oral care protocols increases the chances of achieving good clinical outcomes for individual with diabetes.

Dental hygiene care should not be provided when blood glucose levels are <70 and >240 mg/dL.

When administering local anesthetics, use lowest dose and lowest concentration of a vasoconstrictor that produces desired effect because epinephrine is an insulin antagonist capable of raising blood glucose. Monitor client for signs of hyperglycemia.

A client with well-controlled diabetes with no evidence of infection does not require prophylactic antibiotic premedication.

CRITICAL THINKING EXERCISES

1. Find evidence-based information on the Internet about periodontal disease and diabetes that can be used to educate clients.

2. Review the office emergency kit. What in the emergency kit would be used if the diabetic client were to become disoriented and confused and to report that he took his insulin but did not have time to eat breakfast?

3. At the local pharmacy, purchase glucose tablets that can be kept in the treatment areas. When would these glucose tablets be indicated?

4. Read the following scenario and dental hygiene care plan, and answer the questions that follow.

Client with Diabetes

Bettie Douman is a 40-year-old professional secretary employed full-time at a large university. She has had type 1 diabetes mellitus for 20 years. Bettie has been using the insulin pump for 2 years, which has greatly lowered her blood glucose levels. Her 24-hour blood sugar test results average 180 mL/dL, and 3-month HgA_1c was 8%. Bettie walks the family dog at a fast pace every evening for 30 minutes. She is embarrassed that she has not been careful about eating a nutritionally balanced diet in the last year and a half. On examination the dental hygienist notes low risk for dental caries, generalized moderate gingival bleeding on probing, with localized 4- and 5-mm pocket depths in the molar areas.

What changes would you make, if any, in the following dental hygiene care plan? (See next column.)

What emergency would you prepare for when treating this client? What steps would you take to prevent this emergency?

Develop a detailed self-care plan for this client.

Dental Hygiene Diagnosis	Goal or Expected Behavior
Unmet need for conceptualization and problem solving	By 12/1, client explains the role of oral biofilm in causing periodontal disease.
Unmet need for responsibility for oral health	By 12/1, client verbalizes the role of oral infection in glycemic control.
Client reports improvement in hyperglycemia through the control of periodontal disease	By 1/1, client decreases bleeding points by 75%.

Dental Hygiene Interventions

1. Present “bleeding gums” as an indicator of a bacterial infection that further complicates glycemic control; explain diabetes as a risk factor for periodontal disease.

2. Demonstrate oral biofilm control measures.

3. Discuss antimicrobial agents for control of plaque and inflammation and technique for application.

4. Scale and root debride with ultrasonic instrumentation.

5. Consult with dentist regarding possible systemic doxycycline therapy.

6. Monitor oral health behavior through frequent evaluation.

7. Schedule follow-up evaluation.

Evaluative Statements

1. Client explains interrelationship of diabetic control and periodontal infection.

2. Client demonstrates oral health behavior congruent with maintenance of glycemic control.

3. Client decreases gingival bleeding by 75% to enhance glycemic control.

Dental Hygiene Diagnosis	Goal or Expected Behavior
Unmet need for skin and mucous membrane integrity of the head and neck (undernutrition and increased frequency of carbohydrate consumption)	By 2/1, client verbalizes need for adequate nutrition. By 2/1, client participates in dietary counseling. By 4/1, client increases nutrients in diet.

Dental Hygiene Interventions

1. Relate nutritional needs for diabetes control and integrity of periodontium.

2. Relate frequency of eating to need for oral biofilm control.

3. Relate importance of healthy dentition and periodontium to optimal diet consumption and glycemic control.

4. Design oral biofilm control measures consistent with frequency of carbohydrate consumption.

5. Refer to certified diabetes educator for dietary prescription and meal planning.

Evaluative Statements

1. Client reports normal blood glucose levels.

2. Client indicates compliance with individual dietary prescription and meal plan.