Inside Dental Assisting
Mar/Apr 2011
Volume 7, Issue 2


The metabolic disorder poses numerous significant challenges when caring for a dental patient. Here’s what you need to know.

Diabetes mellitus is a metabolic disease that is characterized by the loss of glucose control and faulty fat and protein metabolism, due to a defect in insulin secretion, insulin action, or both.1 There are several subtypes of diabetes, but the most prevalent—and which will be seen most in the dental setting—are type 1, type 2, and gestational diabetes.1,2 The majority of patients with diabetes have type 2 (85% to 90%), which is marked by decreased insulin action and a relative deficiency in insulin secretion. Another estimated 5% have type 1 diabetes, which is caused by an absolute defect in insulin secretion.3 Gestational diabetes, also called pregnancy diabetes, is similar to type 2, and is especially concerning because it is a risk for maternal and fetal health, and increases risk of developing long-term type 2 diabetes.3

Why is normal insulin action and secretion so important? Insulin, a hormone produced by the pancreas, facilitates the transport of glucose into cells, and is intimately involved with almost every metabolic process and endocrine pathway, because all tissues can use glucose as a substrate for energy production. Insulin-assisted transport of glucose into cells is particularly important in the brain, because brain cells use only glucose for energy.2,4 When insulin secretion or action is hindered, there is decreased glucose clearance from the body, triggering inflammation and placing a significant burden on all key organs. This can result in many complications that significantly affect quality of life.5

Diabetes and Oral Infection: A Reciprocal Relationship

The most pertinent of these complications to dental practice is periodontal disease. Research in the past decade has uncovered a mutually reciprocal relationship between blood sugar control and oral health.6-8 People with diabetes—or its subclinical form of pre-diabetes—and women with gestational diabetes are more likely to have periodontal disease, oral yeast infections, dry mouth, reduced salivary flow, caries, dental abscesses, tooth loss, and slow wound healing (which can pose problems even after common procedures like dental cleaning).6-8 There is also a "dose-response" relationship, in which worsening blood sugar control causes more adverse effects on periodontal health, while controlling blood glucose levels has been found to reduce periodontal infection risk.9 Reciprocally, a healthy person who develops a chronic periodontal infection increases their risk for developing diabetes, and in people with diabetes, periodontal infection worsens blood sugar control and exacerbates diabetes complications and outcomes. Notably, taking measures to reduce periodontal infection enhances blood sugar control.6-8

Behind the mutually reciprocal relationship between diabetes and periodontal infections: Inflammation.10-13 Each of these conditions increases inflammatory compounds in the body, such as C-reactive protein (CRP), interleukin-1 and -6 (IL-1, IL-6), and tumor necrosis factor-alpha (TNF-alpha).14 The presence of these inflammatory compounds in the body has been linked to several health outcomes, including risk of periodontal infection, poor glucose control, degradation of connective tissue, and increased bone loss.10-14

Dental Professionals Can Help Manage Diabetes in Their Patients

Up to 84% of diabetes patients are aware of their risk for oral/periodontal disease, and despite the overwhelming evidence of its benefit, dental care does not appear to be a priority for diabetic patients.15-16 Recent studies have found that dental healthcare workers could play a major role in the management of the diabetic patient, as well as in screening patients with unrecognized diabetes or pre-diabetes.

Diabetes Epidemiology

Diabetes is one of the most common chronic illnesses. According to Centers for Disease Control statistics released in January 2011, 26 million Americans now have diabetes—up 2 million since 2008. In addition, the report reveals that 27% those with the condition are unaware they have it, presenting to healthcare providers after the point of no return in preventing complications.17 While incidence of the disease is rapidly growing across all socioeconomic status and age groups (and at an alarming rate among children), the highest rates are seen in the elderly and minority populations, particularly Hispanics, African Americans, and Native Americans.17 Lately, more attention has been given to pre-diabetes, which applies to individuals with higher-than-normal glycemic levels that aren’t high enough to meet criteria for a diabetes diagnosis. This condition affects 79 million Americans ages 20 and over—up more than 20 million since 2008, with this dramatic rise being linked to increasing rates of overweight and obesity.17

What Are the Risk Factors of Diabetes?

Type 1 Diabetes

This is an autoimmune disorder, in which the body’s own immune cells destroy the insulin-producing beta-cells of the pancreas, and antibodies are directed against insulin itself.19 While there is a genetic component to the disease—differences on chromosome 6 are associated with increased risk of type 1—more than 85% of people who develop it do not have first-degree relatives with the disease, and studies show the risk for an identical twin developing it is a relatively low 30% to 50%, suggesting the influence of environmental factors.18,19

Type 2 Diabetes

This type is considered to evolve in two stages: Stage 1 is the development of slightly impaired glucose control, called pre-diabetes, and Stage 2 is the development of full-blown diabetes.17,20 Pre-diabetes is associated with insulin resistance (IR), a condition in which glucose is less efficiently taken into cells, keeping blood sugar higher than normal. Factors such as overweight/obesity, inactivity, a sugar-rich diet, menopause, and some medications are linked to IR. An individual is able to maintain normal blood sugar levels as long as their pancreas can produce sufficient insulin to manage the high blood sugar. However, for some people the beta-cells eventually lose their ability to increase insulin production to the levels required to compensate for insulin resistance.17,20 This is called beta-cell exhaustion, resulting in pre-diabetes and progressing to diabetes. Aging also increases the odds of experiencing beta-cell exhaustion. As a result, half of people over 65 have pre-diabetes, and 27% have full-blown diabetes.17 There is also a genetic component to type 2, with several risk factors, such as intrabdominal obesity and insulin resistance being under genetic control, and a concordance rate of 90% in identical twins, suggesting much higher heritability than type 1.21

Gestational Diabetes (GD)

This type of diabetes develops in the second trimester of pregnancy, and usually resolves at the end of pregnancy. It is estimated to affect 4% to 10% of pregnancies in the United States. Women who are over 25, overweight or obese before becoming pregnant, have a first-degree relative with type 2 diabetes, who consume a diet high in sugars and refined carbohydrates during pregnancy, and are from a higher-risk ethnic group, such as African Americans, Hispanics, or Native Americans, are more likely to develop GD.17,20 Approximately 50% of women with GD will have a recurrence in future pregnancies, and 30% to 60% develop type 2 diabetes long-term.3


Both types of diabetes have unique, specific symptoms that, when several are exhibited together, should prompt the healthcare professional to ask the patient probing questions about their health status, including whether they’ve been tested for the disease.

According to the American Diabetes Association (www.diabetes.org/diabetes-basics/symptoms) the symptoms of type 1 diabetes include frequent urination, unusual thirst, extreme hunger, unusual or unexplained weight loss, and extreme fatigue and irritability. The symptoms of type 2 diabetes include all of the same symptoms as would be found in type 1, plus frequent infections, blurry vision, cuts and/or bruises that are slow to heal, tingling and/or numbness in the hands and/or feet, and recurring skin, gum or bladder infections. It is important to note, however, that often people with type 2 diabetes have no symptoms at all.


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2. Buse JB, Polonsky KS, Burant CF. Type 2 diabetes mellitus. In: Kronenberg HM. Melmed S, Plonsky KS, Larsen RP, eds. Williams Textbook of Endocrinology. 11th ed. St Louis, MO: W.B. Saunders Company;2008:1329-1330.

3. Kidambi S, Patel S. Diabetes mellitus: A medical overview. In: Genco RJ, Williams R, eds. Periodontal Disease and Overall Health: A Clinician’s Guide. Yardley, PA: Professional Audience Communications Inc; 2010:55-82.

4. Bouché C, Serdy S, Khan CR, Goldfine AB. The cellular fate of glucose and its relevance in Type 2 diabetes. Endocr Rev. 2004;25(5):807-830.

5. Brown GK. Glucose transporters: Structure, function and consequences of deficiency. J Inherit Metab Dis. 2000;23(3):237-246.

6. Grossi SG, Skrepeinski FB, DeCaro T, et al. Treatment of periodontal disease in diabetics reduces glycated hemoglobin. J Periodontol. 1997;68(8):713-719.

7. Demmer RT, Jacobs DR, Desvarieux M. Periodontal disease and incident type 2 diabetes : Results from the First National Health and Nutrition Examination Survey and its Epidemiological Follow-Up Study. Diabetes Care. 2008;31(7):1373-1379.

8. Tsai C, Hayes C, Taylor GW. Glycemic control of type 2 diabetes and severe periodontal disease in the US adult population. Community Dent Oral Epidemiol. 2002;30(3):182-192.

9. Mealey BL, Ocamp GL. Diabetes mellitus and periodontal disease. Periodontol 2000. 2007;44:127-153.

10. Lamster IB, Lalla E, Borgnakke WS, Taylor GW. The relationship between oral health and diabetes mellitus. JADA. 2008;139(Suppl):19S-24S.

11. Taylor GW, Borgnakke WS. Periodontal disease: associations with diabetes, glycemic control and complications. Oral Dis. 2008;14(3):191-203.

12. Silva JA, Lorencini M, Reis JR, Carvalho HF, et al. The influence of type I diabetes mellitus in periodontal disease induced-changes of the gingival epithelium and connective tissue. Tissue Cell. 2008;40(4):283-292.

13. Gyurko R, Siquiera CC, Caldon N, et al. Chronic hyperglycemia predisposes to exaggerated inflammatory response and leukocyte dysfunction in Akita mice. J Immunol. 2006;177(10):7250-7256.

14. Loos BG. Systemic markers of inflammation in periodontitis. J Periodontol. 2005;76(Suppl):2106-2115.

15. Sandberg GE, Sundberg HE, Wikblad KF. A controlled study of oral self-care and self-perceived oral health in type 2 diabetic patients. Acta Odontol Scand. 2001;59(1):28-33.

16. Tomar SL, Lester A. Dental and other health care visits among US adults with diabetes. Diabetes Care. 2000;23(10):1505-1510.

17. Centers for Disease Control and Prevention. National Diabetes Fact Sheet, 2011. https://www.cdc.gov/diabetes/pubs/pdf/ndfs_2011.pdf. Accessed January 28, 2011.

18. Eisenbarth GS, Polonsky KS, Buse JB. Type I diabetes mellitus. In: Kronenberg HM. Melmed S, Plonsky KS, Larsen RP, eds. Williams Textbook of Endocrinology. 11th ed. St Louis, MO: W.B. Saunders Company;2008:1393-1396.

19. Kaprio J, Tuomilehto J, Koshenvuo M, et al. Concordance for type I and type 2 diabetes mellitus in a population-based cohort of twins in Finland. Diabetologia. 1992;35(11):1060-1104.

20. American Diabetes Association. Diagnosis and classification of diabetes mellitus. Diabetes Care. 2008;31(Suppl):S55-S60.

21. Bowden DW, Sale M, Howard TD, et al. Linkage of genetic markers on human chromosomes 21 and 12 to NIDDM in Caucasian sib pairs with a history of diabetic neuropathy. Diabetes. 1997;46:882-886.

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