“Do you have any sugar-free candy?” The question came from directly in front of me and startled me. I snapped my head up to see who was asking.
“Looks like you might have had too much sugar,” she said with a laugh as she acknowledged my rapid head movement. Her breath was heavy and pungent, a mixture of the aroma of ripened fruit with a trace of ammonia.
Then she smiled. There it was. A single anterior tooth, extending from her mandible to her upper lip, was proudly standing there 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.
Then she opened her eyes as wide as she could, looked at me through her thick eyeglasses, and pointed to her last remaining anterior tooth. “Well, I guess it must be this one!” she said with a laugh.
As I laughed with her, I couldn’t help but think about the implications of what she said. That “sweet tooth,” as she called it, was her rationale for consuming sugary treats through the years. It was probably also the reason why she developed obesity, periodontal disease, and ultimately, diabetes mellitus and chronic kidney disease.
Diabetes mellitus is a chronic debilitating condition that 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.
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 that block glucose transport at the cellular level.
As a result of insulin resistance, glucose remains in the blood instead of being used 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 bloodstream. This leads to abnormal production of glucose from glycogen, fat, and protein, which worsens hyperglycemia. The 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 quit 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. These include 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 patients increase their food intake, they lose weight.
Hyperglycemia also accelerates the formation of atherosclerotic plaques, which increases the risk of hypertension, myocardial infarction, and stroke. 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 can lead to the development of neuropathies that occur in the peripheral nervous system. This may lead to muscle weakness, burning sensations and numbness (diabetic peripheral neuropathy), gastrointestinal dysfunction (especially diabetic gastroparesis), or bladder and bowel dysfunction (incontinence).
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), 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.
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.
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 who have few teeth, dentures, or chronic mouth pain prefer food that requires minimal chewing and can be easily swallowed. These foods are often high in simple carbohydrates and fat, and low in fiber. Therefore, these patients are at risk for deficiencies of certain nutrients. Poor nutrition impairs the proper development of oral cavity tissues and compromises healing.
Poor nutrition also compromises 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.
Measuring 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 measure patients’ levels 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 during the preceding two to three months.
Managing type 2 diabetes involves lifestyle modifications such as 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 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 designed to reduce hyperglycemia and insulin resistance. These were 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). The side effects include hypglycemia and weight gain.
• Insulin sensitizers include the biguanides, such as metformin, which works primarily in the liver to suppress glucose production, and 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 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 GI 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 use processes that our body already employs to normalize blood glucose after eating.
• Exenatide (Byetta), liraglutide (Victoza), and dulaglutide (Trulicity) are incretin agonists that 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 can be taken orally (not injected), and they 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.
Epinephrine may cause an elevation in blood glucose and could exacerbate comorbid cardiovascular disease.
Dental hygienists are in a unique position to identify undiagnosed cases of type 2 diabetes mellitus. Patients who present with signs and symptoms of the condition (polyuria, polydipsia, polyphagia, and weight loss) should be referred for medical consultation. Those who keep their diabetes under good control and who have no complications should not require any 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 any signs, such as fever and swelling. While diabetic patients usually tolerate the use of local anesthesia with 1:100,000 epinephrine well, epinephrine may cause an elevation in blood glucose and could exacerbate comorbid cardiovascular disease.
I spent time with my new patient discussing 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. I strongly encouraged her to call her medical office and dental office and make appointments for reassessment and evaluation. I counseled her about the importance of good oral hygiene to avoid future complications. I urged her to follow the instructions of her dental hygienist for proper home care, and to schedule routine follow-up appointments so her hygienist could monitor her progress.
She politely and intently listened to all that I had to say. When I was finished, I asked if she had any questions. “Yes, I do. You never did tell me where you keep the sugar-free candy.”
THOMAS A. VIOLA, RPH, CCP, In addition to his daily practice of the profession of pharmacy, Thomas A. Viola, RPh, CCP, also serves the professions of dentistry, dental hygiene, and dental assisting as an educator, published writer, and professional speaker. As an educator, Viola is a member of the faculty of seven dental hygiene and dental assisting programs, as well as several national board exam review courses. Visit Viola’s website: www.tomviola.com.