Diabetes mellitus affects more than 12 million people in the U.S. Diabetes mellitus is a clinical syndrome characterized by hyperglycemia due to an absolute or relative deficiency of insulin, and is characterized by metabolic abnormalities and long-term complications involving the eyes, kidneys, nervous system, vasculature, and periodontium. Diabetes is commonly categorized as type 1, or insulin dependent, and type 2, non-insulin dependent.

It is well established that diabetics are more likely to develop periodontal disease than non diabetics with disease severity being related to the duration of diabetes. Although the precise etiology is still uncertain in both main types of primary diabetes, and environmental factors can interact with a genetic susceptibility to determine which individual with a genetic predisposition may actually develop the clinical syndrome, and the timing of its onset.

Environmental factors in insulin-dependent diabetes include virus, diet, immunological factors, and pancreas disease. In non-insulin-dependent diabetes, environmental factors such as lifestyle, age, pregnancy, pancreas pathology, and insulin secretion and resistance are included.

Recently, periodontitis has been called “the sixth complication of diabetes mellitus”, being twice as prevalent in diabetic individuals compared to non-diabetics. Severe periodontal disease often coexists with severe diabetes mellitus; and diabetes is also a risk factor for severe periodontal disease. Experimentally produced periodontitis has been shown to increase blood glucose levels in uncontrolled diabetic animals, increase insulin resistance in diabetic patients and their associated micro- and macro-vascular complications and to amplify the magnitude of the advanced glycation end product (AGE)-mediated cytokine response operative in diabetes mellitus. Studies have reported that the treatment of periodontitis can improve glycemic control, thus lowering blood glucose levels.

The concentration of glycated hemoglobin in serum is a direct function of the time that hemoglobin is exposed to elevated glucose levels.  A longitudinal study of diabetes and periodontal disease has been carried out in the Pima tribe, an Indian population inthe United States having a 50% prevalence of non-insulin-dependent diabetes, the highest in the world. The results indicated that severe periodontitis at baseline is associated with increased risk of poor glycemic control, that is glycated hemoglobin of 9% or more, at a follow-up visit two or more years later. These findings suggest that severe periodontitis may be an important risk factor in the progression of diabetes, and control of periodontal infection is essential to achieve long-term control of diabetes mellitus.

The exact cellular and molecular basis for diabetic periodontitis is unknown. However, recent evidence suggests that periodontitis and delayed dermal wound healing may be manifestations of the same general systemic deficit in diabetes that involve cellular and molecular signal impairment through macrophage phenotype alterations, along with dysregulation of cytokines at the wound site. Also, individuals with hyperglycemia, in combination with high levels of serum low density lipoproteins and triglycerides, have been shown to the have increased levels of advanced glycation end products (AGEs) which may alter their macrophage phenotypes. This may be responsible for dysregulation of macrophage cytokine production and increased inflammatory gingival tissue destruction and alveolar bone loss.

One possible biologic mechanism for why diabetics have more severe periodontal disease is that glucose-mediated AGE accumulation affects the migration and phagocytic activity of mononuclear and polymorphonuclear phagocytic cells, resulting in the establishment of a more pathogenic subgingival flora. The maturation and gradual transformation of the subgingival microflora into an essentially gram-negative flora will in turn constitute, through the ulcerated pocket epithelium, a chronic source of systemic challenge. This in turn triggers both an “infection-mediated” pathway of cytokine upregulation, especially with secretion of TNF- and IL-1, and a state of insulin resistance, affecting glucose-utilizing pathways. Thus, monocytes in diabetic individuals may be “primed” by AGE-protein binding. The interaction of mononuclear phagocytes with AGE-modified proteins induces upregulation of cytokine expression and induction of oxidative stress.

A model was presented by Grossi and Genco in 1998, in which severe periodontal disease increases the severity of diabetes mellitus and complicates metabolic control. They proposed that an infection-mediated upregulation cycle of cytokine synthesis and secretion by chronic stimulus from LPS and products of periodontopathic organisms may amplify the magnitude of the advanced glycation end product (AGE)-mediated cytokine response that is operative in diabetes mellitus. Simultaneously, periodontal infection may induce a chronic state of insulin resistance, contributing to the cycle of hyperglycemia, nonenzymatic irreversible glycation, and AGE-protein binding and accumulation, amplifying the classical pathway of diabetic connective tissue degradation, destruction, and proliferation. Hence, the relationship between diabetes mellitus and periodontal disease or infection becomes two-way. A self-feeding two-way system of catabolic response and tissue destruction ensues, resulting in more severe periodontal disease and increased difficulty in controlling blood sugar.

The fundamental derangement in insulin-dependent diabetes is the hypo-production of insulin due to destruction of the beta cells of the pancreas. In non-insulin-dependent diabetes, the derangement involves resistance of target tissue to insulin action.

Dysesthia (Oral Burning)

Patients with diabetes may complain of continuous burning sensation, usually involving the tip and dorsum of the tongue or the palate, and other underlying mucosal disorders, such as lichen planus and candidiasis, needs to be addressed and treated in these individuals, in order to treat the burning sensation. Oral burning may also be a sign of vitamin B12 and/or zinc deficiencies. The levels of these nutrients should be examined and corrected if they are found to be abnormal. Oral burning in the absence of physical and biochemical changes may represent a diabetes-related oral sensory neuropathy. If physical or biochemical abnormalities cannot be found, the symptoms of burning mouth can be improved using neuropathic analgesic medications such as a tricyclic antidepressant or clonazepam. However, a side effect or these medications is xerostomia, which may compound any existing alterations in saliva and increase the risk of candidiasis (a fungal infection) and dental caries.

Dysgeusia (Altered Taste Sensation)

Dysgeusia may occur in individuals with diabetes and may adversely affect food choices and intake of nutrients. Altered taste in individuals with diabetes is often caused by altered salivary chemistry, secondary to the diabetes being out of control.  Xerostomia, burning mouth and tongue, and/or candidiasis, should all be explored to determine any possible underlying disorder. Possible therapies for relief from dysgeusia have included the use of increased flavoring agents during food preparation, substituting alternative protein sources if the individual is unable to tolerate meat products, and the use of artificial saliva when needed.

Dietary Recommendations

Chemotherapy, radiation, cancer by itself, diabetes, or other diseases and medications may cause food to taste different than your previous taste experiences. These individuals can modify their diet and continue to eat healthy balanced meals. To enhance flavor these individuals can: 1) marinate meat in a variety of sauces, such as soy, barbeque, and sweet-n-sour sauce, or salad dressing; 2) Use a variety of seasonings on vegetables such as garlic powder, lemon juice/lemon pepper, and basil; and 3) use fresh fruit or vanilla extract to enhance the flavor of milk shakes, ice cream and pudding. In order to minimize the metallic taste of food these in individuals should use plastic utensils. Also, tart foods such as citrus juices, pickles, relish, grapefruit, cranberry, and Granny Smith apples, can help these individuals overcome the metallic taste of food. If red meat tastes unusual, other protein sources can include chicken, turkey, fish, and dairy products. The addition of sugar can improve the flavor of salty foods (Warning: some diets involve salt and sugar restrictions). Other suggestions are: 1) serve foods cold or at room temperature to reduce their odors; 2) use a variety of foods to complement your taste preferences; and 3) serve foods attractively and in a pleasant atmosphere to enhance the individual’s acceptance.