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Sweet Tooth: Knowledge about type 2 diabetes and the drugs used to treat it can help you better care for patients.

"Do you have any sugar-free candy?" a patient asked her dentist. Her breath was heavy and pungent, with a mixture of the aroma of ripened fruit and a trace of ammonia. Then, she smiled and there it was: a single anterior tooth, extending from her mandible to her upper lip, standing proudly all by itself, like a lone survivor of a great battle. Her lack of any other anterior dentition was obvious on her face and in her speech.

"My doctor says I have to go easy on the candy now that I have diabetes," she said with a chuckle. "But, I can't help it if I have a sweet tooth!" She opened her eyes as wide as she could and pointed to her last remaining anterior tooth. "Well, I guess it must be this one!" she laughed.

Unfortunately, that "sweet tooth," as she called it, was her rationale for consuming sugary treats over the years. And, it might also be the reason why she developed obesity, periodontal disease, and, ultimately, diabetes mellitus and chronic kidney disease.

Diabetes mellitus is a chronic debilitating condition, which leads to a variety of complications, such as microvascular disease, atherosclerosis, neuropathy, retinopathy, and nephropathy. Type 2 diabetes mellitus is the most prevalent type of diabetes mellitus.

What Happens in the Body

Glucose in the blood stimulates the pancreatic beta cells to secrete insulin. Insulin remains in circulation for only a few minutes. Its primary function is to interact with insulin receptors on target tissues, such as muscle and fat, to activate glucose transport proteins. Resistance to insulin at these receptors is the hallmark of type 2 diabetes. The most common cause of this insulin resistance is obesity. Adipocytes (fat cells) release free fatty acids, which block glucose transport at the cellular level.

As a result of insulin resistance, glucose remains in the blood instead of being utilized by the cells. This results in hyperglycemia. Since the cells cannot transport glucose in to meet their own metabolic needs, the cells starve. In response, the cells release mediators to stimulate the liver to produce and release more glucose into the blood stream. This leads to abnormal production of glucose from glycogen, fat, and protein, further worsening hyperglycemia. Now that extra glucose in the bloodstream continues to stimulate the pancreatic beta cells to secrete insulin and the vicious cycle continues. Eventually, as with Type 1 diabetes, the pancreatic beta cells fail and cease producing insulin. However, in type 2 diabetes, this process is insidious and takes place over many years.

Systemic complications of diabetes mellitus result from prolonged hyperglycemia and pathologic microvascular and macrovascular changes that occur, including thickening of the intima, endothelial proliferation, and atherosclerosis. While these pathologic vascular changes may affect the whole body, they are especially damaging to the retinas and kidneys, many times resulting in blindness and renal failure.

Hyperglycemia results in glucose excretion in the urine, which leads to increased volumes of urine voided. This polyuria depletes extracellular fluids and reduces the secretion of saliva. Dehydration occurs and results in increased thirst, or polydipsia. In addition, cellular starvation leads to weight loss and increased hunger, or polyphagia. Although the patient increases his or her food intake, the patient continues to lose weight.

Hyperglycemia also accelerates the formation of atherosclerotic plaques, which increases the risk of hypertension, myocardial infarction, and stroke in diabetic patients. In addition, hyperglycemia contributes to increased susceptibility to infection and poor wound healing. Thus, diabetes mellitus is often associated with decubitus ulcerations and gangrenous extremities that may require amputation. Finally, hyperglycemia also leads to the development of neuropathies that occur in the peripheral nervous system. This may lead to diabetic patients experiencing muscle weakness, burning sensations and numbness (diabetic peripheral neuropathy), gastrointestinal dysfunction (especially diabetic gastroparesis), and bladder and bowel dysfunction (incontinence).

Oral Complications

Oral complications of diabetes mellitus include xerostomia (due to dehydration and reduced secretion of saliva), increased susceptibility to bacterial, viral, and fungal infections (due to altered immune response), and increased incidence and severity of caries; and gingivitis and periodontal disease (due to enhanced inflammatory responses, poor wound healing, and microvascular changes). Oral lesions are common in diabetic patients (especially periapical abscesses and lichen planus). Due to pathologic changes involving nerves in the oral cavity, diabetic neuropathy may result in oral paresthesia, pain, and burning mouth symptoms,

The interplay between diabetes, periodontal disease and systemic inflammation is complex. Patients who use medications to treat their diabetes mellitus believe they must eat frequent, small meals throughout the day to prevent hypoglycemia. This has a negative impact on the teeth, due to the constant supply of sugary foods to the bacteria in the mouth. Patients with diabetes mellitus have decreased saliva and are less able to clear away food particles. This further increases the contact time of ingested carbohydrates with the bacteria in the mouth.

Patients with diabetes mellitus with few teeth or who have dentures, or who have chronic mouth pain prefer food that is easily swallowed with minimal chewing. These foods are often high in simple carbohydrates, low in fiber, and high in fat. Thus, these patients are at risk for deficiencies of certain nutrients. Poor nutrition impairs the proper development of the tissues of the oral cavity and compromises healing.

Poor nutrition also compromises the immune response and decreases the ability to modulate inflammatory response. Periodontal disease induces inflammatory cells to migrate to the oral cavity. After tooth brushing or flossing, the bacteria and inflammatory mediators enter the systemic circulation, leading to chronic systemic inflammation, which may result in the development of insulin resistance and atheroma formation.

Diabetes Management

Measurement of blood glucose via self-testing kits is critical to the diagnosis and management of diabetes mellitus. However, since daily blood glucose levels may be influenced by various factors, such as diet and physical activity, we also often measure a patient's level of glycosylated hemoglobin A. This "A1C" test is useful in determining the long-term level of control of hyperglycemia in patients with diabetes, since it reflects blood glucose levels over the preceding 2 to 3 months.

The management of type 2 diabetes involves lifestyle modifications, including nutritional therapy for weight loss and regular exercise. Unfortunately, the benefits of therapeutic lifestyle modifications as the sole approach to treatment are short-lived since many patients have difficulty in implementing and maintaining those lifestyle changes. In addition, over time, blood glucose control deteriorates due to the progressive loss of pancreatic beta cell function.

While we often think of type 2 diabetes as non-insulin dependent, in many cases, type 2 diabetics do indeed use insulin to control hyperglycemia. While insulin may ultimately be necessary, treatment of type 2 diabetes usually begins with a non-insulin medication treatment regimen.

Historically, type 2 diabetes was treated with non-insulin medications aimed at reducing hyperglycemia and insulin resistance, such as insulin secretagogues, insulin sensitizers, and drugs that impair absorption of ingested carbohydrates.

* Insulin secretagogues work by stimulating insulin secretion from the pancreatic beta cells. These include sulfonylureas, such as glipizide and glimepiride, and glinides, such as repaglinide (Prandin) and nateglinide (Starlix). Side effects of these medications include hypoglycemia and weight gain.

* Insulin sensitizers include the biguanides, such as metformin, which works primarily in the liver to suppress glucose production, and the thiazolidinediones (TZDs), such as pioglitazone (Actos) and rosiglitazone (Avandia), which increase insulin sensitivity of muscle and adipose tissue. Side effects of metformin include a metallic taste and side effects of the TZDs include weight gain and fluid retention (which may worsen comorbid cardiovascular disease).

* Alpha-glucosidase inhibitors (AGIs), such as acarbose (Precose) and miglitol (Glyset), block the absorption of ingested carbohydrates in the small intestine. Side effects of these medications include Gl upset.

New non-insulin treatments for type 2 diabetes mellitus include the use of incretin modulators. Incretins are gastrointestinal hormones that increase insulin release from beta cells in the pancreas, while also inhibiting glucagon secretion and slowing absorption of carbohydrates. Thus, incretin modulators are very useful in management of type 2 diabetes, since they utilize processes that our body already employs to normalize blood glucose after eating.

* Exenatide (Byetta), liraglutide (Victoza) and dulaglutide (Trulicity) are incretin agonists which mimic the actions of the incretin hormones. They are injected subcutaneously. Side effects include increased risk of pancreatitis.

* Sitagliptin (Januvia), saxagliptin (Onglyza), linagliptin (Tradjenta) and alogliptin (Nesina) are inhibitors of DDP-4, an enzyme responsible for breakdown of incretin hormones. By inhibiting this enzyme, DDP-4 inhibitors prolong the action of the incretin hormones. The key advantages of these drugs are that they have relatively few side effects, they are taken orally (not injected) and, typically, cause less hypoglycemia than other treatments.

The most controversial non-insulin medications used in the treatment of type 2 diabetes are the SGLT2 inhibitors. Canagliflozin (Invokana), dapagliflozin (Farxiga), and empagliflozin (Jardiance) work by inhibiting reabsorption of glucose in the kidney, which results in lower blood glucose. However, these medications have been linked to an increased risk of serious adverse effects, such as ketoacidosis, kidney damage, bone fractures and lower limb amputations.

Signs and Symptoms

Dental assistants are in a unique position to identify undiagnosed cases of type 2 diabetes mellitus. Patients with undiagnosed type 2 diabetes mellitus who present with signs and symptoms of the condition (polyuria, polydipsia, polyphagia, and weight loss) should be referred for medical consultation. Patients with type 2 diabetes mellitus under good control and with no complications require no specific dental care planning.

However, patients with complications, such as renal disease or cardiovascular disease, may require specific dental treatment plan alterations. Diabetic patients undergoing oral surgical procedures are at increased risk of infection and should be monitored closely for its signs (such as fever and swelling). While the use of local anesthesia with 1:100,000 epinephrine is generally well tolerated in diabetic patients, epinephrine may cause an elevation in blood glucose and could also exacerbate comorbid cardiovascular disease.

Spend some time to talk with patients about the merits of sugar-free candy, the complications of uncontrolled type 2 diabetes, the latest recommendations for diet and exercise, and the newest medications and blood glucose self-testing kits available. Encourage patients with diabetes or diabetes symptoms to contact their medical offices to make appointments for reassessment and evaluation. And be sure to counsel patients about the importance of good oral hygiene in avoiding future complications.

By Thomas Viola, RPh, CCP

Thomas Viola, RPh, CCP, is a clinician, educator, speaker, and author in the area of dental pharmacology/local anesthesia. Reach him at 609.504.9252 or
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Author:Viola, Thomas
Publication:The Dental Assistant
Geographic Code:1USA
Date:Sep 1, 2017
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