Clinical Update



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Clinical Update


Naval Postgraduate Dental School

National Naval Medical Center

8901 Wisconsin Ave

Bethesda, Maryland 20889-5600


Vol. 29, No. 1

2007

Diabetes mellitus and periodontal disease: a two-way street through health and disease

Lieutenant Commander John H. Wilson, DC, USN and Commander Matthew J. Gramkee, DC, USN




Introduction

Diabetes Mellitus (DM) affects roughly 12 million people in the US; as many as half of these people may be unaware of their condition. Two forms of the disease exist. Type I DM (formerly Insulin Dependent Diabetes Mellitus) is a result of destruction of the Islet of Langerhan cells in the pancreas, resulting in a lack of endogenous insulin production. Type II DM (formerly Non-Insulin Dependent Diabetes Mellitus) comprises 85-90% of diabetes cases, and is a result of impaired insulin receptors on the target cells.1 Periodontal disease includes a spectrum of plaque-induced, inflammatory conditions affecting gingiva, cementum, and alveolar bone. Estimates of the prevalence of gingivitis in the US range from 39-60%, while only 5-15% of the population suffers from severe generalized periodontitis.2 The purpose of this clinical update is to present an evidence based review of the effects of diabetes on the clinical course of periodontal disease, as well as to argue the importance of achieving periodontal health in the overall management plan for both type I and type II diabetics.


Diagnosis and medical management of diabetes

The signs and symptoms of DM are the classic triad of polyuria, polydipsia, and polyphagia, together with pruritis, weakness, and fatigue. Physicians rely on a battery of tests to diagnose DM, including fasting blood glucose, oral glucose tolerance test, and casual plasma glucose (fasting not required). One particularly useful test to determine the level of metabolic control is the glycated hemoglobin A1c, or HbA1c. This measures the percentage of glycated hemoglobin moieties on red blood cells. The HbA1c gives a measure of the blood glucose status over the half-life of the RBC, which is about 30-90 days.1 Metabolic control of DM involves special attention to diet, exercise, weight loss, and multiple pharmacologic agents. Type I diabetics require exogenous insulin. Type II diabetics are usually managed with the use of sulfonylureas such as glipizide or glyburide. These drugs stimulate insulin release from the pancreas, as well as promote insulin uptake in the tissues. Other drugs, such as metformin and troglitazone increase tissue sensitivity to insulin without increasing pancreatic release of insulin, minimizing the risk of a hypoglycemic crisis. Complications of DM are a direct result of hyperglycemia, and include retinopathy (DM is the leading cause of blindness in the US), nephropathy, neuropathy, macrovascular disease, and altered wound healing.3


The sixth complication of diabetes

Numerous cross-sectional and longitudinal studies have identified DM as a risk factor for periodontal diseases.4-9 Ciancola et al.4 looked at the periodontal condition of Type I diabetics, and compared them to non-diabetic controls. While the prevalence of periodontitis among non-diabetics aged 11-18 was only 1.7%, the same age range of diabetics had a prevalence of periodontitis of 9.8%. They also noted an almost linear increase of periodontitis with age, with 39% of subjects over 19 years old exhibiting mild to severe periodontitis. The progression of clinical attachment loss was found to be accelerated in Type I diabetics compared to non-diabetics in a study by Firalti.8 The significant difference was noted despite similar levels of plaque control. Metabolic control of Type I DM has been shown to impact periodontal conditions. Safkan-Seppälä and Ainamo6 demonstrated that poorly controlled Type I diabetics had significantly more clinical attachment loss and alveolar bone loss compared to those Type I diabetics with good glycemic control. The same association holds true for Type II diabetics. Emrich et al.5 looked at the prevalence and severity of periodontal disease in Native Americans. Type II diabetics were found to have an increased risk of destructive periodontitis with an odds ratio ranging from 2.81 (based on clinical attachment loss) to 3.43 (based on alveolar bone loss.) Löe7 found that 8% of non-diabetic Pima Indians under the age of 35 had advanced periodontal disease, versus 48% of Type II diabetics in the same age range. He estimated the diabetics were about three times more likely to exhibit periodontitis. In a longitudinal study, Taylor et al.9 showed that Type II DM was associated with an increased rate of alveolar bone loss progression. Several mechanisms for worsened periodontal status in diabetics have been studied. Bissada et al10 demonstrated both decreased chemotaxis and phagocytosis of PMNs in peripheral blood of diabetics. Derangements of collagen metabolism occur in diabetics. Golub et al.11 showed in vitro and in vivo that collagenase activity is enhanced in diabetic rats. Also, a dose-dependent decrease in collagen production by fibroblasts was noted with increasing glucose concentrations.12 In a hyperglycemic environment, numerous proteins, including collagen, undergo a non-enzymatic glycosylation process to form advanced glycation endproducts (AGEs). AGEs result in a myriad of events, including increased cross-linking and decreased solubility and turnover of collagen. AGEs induce macrophages and monocytes to increase secretion of pro-inflammatory cytokines such as interleukin-1 and tumor necrosis factor-α.3 Zambon et al.13 suggested that both quantitative and qualitative differences in periodontal pathogens could account for increased susceptibility to periodontitis in diabetics. Listgarten et al.14 noted increased thickness of the basement membrane of capillary endothelium in diabetics compared to non-diabetics.
Periodontitis as a risk factor for diabetes

While it is well established that diabetes mellitus is a significant risk factor for periodontitis, researchers are beginning to look at the converse - periodontal infections negatively impacting the glycemic control of both Type I and Type II diabetics. As early as 1960, Williams and Mahan15 noted a significant reduction in insulin requirements in 7 of 9 patients after periodontal therapy. Taylor et al.16 in a seven year longitudinal study of Type II diabetics found that significantly more subjects demonstrated worsening glycemic control who had severe periodontitis. Grossi et al.17 in a randomized clinical trial of Type II diabetic Pima Indians showed that scaling and curettage plus systemic doxycycline was able to reduce HbA1c by almost 10%. More recently, Kuran et al.18 noted an 11% decrease in HbA1c in Type II diabetics after oral hygiene instructions and full mouth scaling and root planing. Slight increases were noted in the control group, receiving only oral hygiene instructions. Both in vitro and animal studies have documented the role of the pro-inflammatory cytokine Tumor Necrosis Factor – α in insulin resistance. Iwamoto et al.19 have shown that non-surgical periodontal therapy significantly reduced both HbA1c and serum TNF-α in thirteen Type II DM patients. They hypothesize that improved glycemic control is achieved by reduction of TNF-α and improved insulin resistance following control of periodontal inflammation. Taken together, the evidence suggests that control of periodontal disease should be an important part of the overall management of patients with DM.


Conclusion

The evidence overwhelmingly supports DM as a risk factor for periodontal disease. There is now a growing body of evidence that points to periodontal infections as an independent risk factor for poor glycemic control in patients with DM. With this knowledge, it is incumbent upon dentists and physicians alike to work together to achieve the desired goal of improvements in patient’s overall health.


References

1. Report of the Expert Committee on the Diagnosis and Classification of Diabetes Mellitus. Diabetes Care. 1997 Jul;20(7): 1183-97.

2. Burt B, Research, Science and Therapy Committee of the American Academy of Periodontology. Position paper: epidemiology of periodontal diseases. J Periodontol. 2005 Aug;76(8): 1406-19.

3. Mealey B. Diabetes and periodontal diseases. J Periodontol. 1999 Aug;70(8):935-49.

4. Cianciola LJ, Park BH, Bruck E, Mosovich L, Genco RJ. Prevalence of periodontal disease in insulin-dependent diabetes mellitus (juvenile diabetes). J Am Dent Assoc. 1982 May;104(5): 653-60.

5. Emrich LJ, Shlossman M, Genco RJ. Periodontal disease in non-insulin-dependent diabetes mellitus. J Periodontol. 1991 Feb; 62(2):123-31.

6. Safkan-Seppälä B, Ainamo J. Periodontal conditions in insulin-dependent diabetes mellitus. J Clin Periodontol. 1992 Jan; 19(1):24-9.

7. Löe H. Periodontal disease. The sixth complication of diabetes mellitus. Diabetes Care. 1993 Jan;16(1):329-34.

8. Firatli E. The relationship between clinical periodontal status and insulin-dependent diabetes mellitus. Results after 5 years. J Periodontol. 1997 Feb;68(2):136-40.

9. Taylor GW, Burt BA, Becker MP, Genco RJ, Shlossman M. Non-insulin dependent diabetes mellitus and alveolar bone loss progression over 2 years. J Periodontol. 1998 Jan;69(1):76-83.

10. Bissada NF, Manouchehr-Pour M, et al. Neutrophil Functional Activity in Juvenile and Adult Onset Diabetic Patients with Mild and Severe Periodontitis. J Periodontal Res. 1982 Sep;17(5):500-2.

11. Golub LM, Schneir M, Ramamurthy NS. Enhanced collagenase activity in diabetic rat gingiva: in vitro and in vivo evidence. J Dent Res 1978 Mar;57(3):520-5.

12. Willershausen-Zönnchen B, Lemmen C, Hamm G. Influence of high glucose concentrations on glycosaminoglycan and collagen synthesis in cultured human gingival fibroblasts. J Clin Periodontol. 1991 Mar;18(3):190-5.

13. Zambon JJ, Reynolds H, Fisher JG, Shlossman M, Dunford R, Genco RJ. Microbiological and immunological studies of adult periodontitis in patients with noninsulin-dependent diabetes mellitus. J Periodontol. 1988 Jan;59(1):23-31.

14. Listgarten MA, Ricker FH Jr, Laster L, Shapiro J, Cohen DW. Vascular basement lamina thickness in the normal and inflamed gingiva of diabetics and non-diabetics. J Periodontol. 1974 Sep;45(9):676-84.

15. Williams RC, Mahan CJ. Periodontal disease and diabetes in young adults. JAMA. 1960 Feb 20;172:776-8.

16. Taylor GW, Burt BA, Becker MP, Genco RJ, Shlossman M, Knowler WC, Pettitt DJ. Severe periodontitis and risk for poor glycemic control in patients with non-insulin-dependent diabetes mellitus. J Periodontol. 1996 Oct;67(10 Suppl):1085-93.

17. Grossi SG, Skrepcinski FB, DeCaro T, Robertson DC, Ho AW, Dunford RG, Genco RJ. Treatment of periodontal disease in diabetics reduces glycated hemoglobin. J Periodontol. 1997 Aug;68(8):713-9.

18. Kiran M, Arpak N, Unsal E, Erdogan MF. The effect of improved periodontal health on metabolic control in type 2 diabetes mellitus. J Clin Periodontol. 2005 Mar;32(3):266-72.

19. Iwamoto Y, Nishimura F, Nakagawa M, Sugimoto H, Shikata K, Makino H, Fukuda T, Tsuji T, Iwamoto M, Murayama Y. The effect of antimicrobial periodontal treatment on circulating tumor necrosis factor-alpha and glycated hemoglobin level in patients with type 2 diabetes. J Periodontol. 2001 Jun;72(6):774-8.


Lieutenant Commander Wilson is a third year Periodontics resident at the Naval Postgraduate Dental School. Commander Gramkee is an associate professor at the Naval Postgraduate Dental School, Department of Periodontics.
The views expressed in this article are those of the author and do not necessarily reflect the official policy or position of the Department of the Navy, Department of Defense, nor the U.S. Government.




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