Public Health Implications of Chronic Periodontal Infections in Adults

Diabetes and Periodontal Disease: Current Concepts
Robert Genco, DDS, PhD, Distinguished Professor, Oral Biology, School of Dental Medicine, State University of New York, Buffalo, New York

Diabetes mellitus appears to be the best studied disease related to periodontal disease. Extensive studies show that individuals with diabetes are more susceptible to periodontal disease than those without diabetes. For example, diabetes mellitus, types 1 and 2, are well established as increasing the risk for severe periodontal disease, with earlier onset among people with diabetes than among others (1, 2, 3).

Recently, the concept has developed that people with both diabetes and periodontal disease suffer from more severe diabetes over time as a result of the systemic effects of periodontal infection. For example, Taylor and colleagues (4) found that people with diabetes who also had periodontal disease suffered from worsened glycated hemoglobin over time than did those diabetics who did not have periodontal disease. This and similar observations led to a series of clinical trials in which periodontal therapy, especially therapy involving adjunctive systemic and/or local antibiotics, was found to be effective in treating periodontal disease in people with diabetes and also resulted in reduction of glycated hemoglobin levels (5). Further studies, especially randomized controlled clinical trials, are required to determine whether the reduction of glycated hemoglobin brought about by resolving periodontal infections in patients with diabetes will result in reducing complications such as retinopathy, nephropathy, and other clinical complications of diabetes.

Other studies have assessed why patients with diabetes respond to periodontal infection with aggravated host destructive responses. One theory (6) suggests that there is a general hyperinflammatory response associated with advanced glycation end products (AGE). This response triggers inflammatory cells through AGE receptors with a release of proinflammatory mediators leading to excessive tissue destruction. This hyperinflammatory response is manifest at the monocyte and neutrophil (cellular) levels. Other mechanisms that explain the increased pathology seen in diabetes patients as a result of periodontal infection include altered vascular physiology (7), reduced immune response, particularly protective response by neutrophils, and reduced ability for tissues to heal.

Many possible theories explain why glycated hemoglobin is reduced when periodontal infections are resolved in diabetes patients. There is some evidence that systemic overflow of tumor necrosis factor-alpha (TNF-alpha) and other inflammatory cytokines from periodontal lesions may act in concert with TNF-alpha from other sources, such as adipocytes, to increase insulin resistance (8). In addition to insulin resistance, it is thought that impaired beta cell function leads to reduced insulin secretion resulting in sustained elevated glucose concentrations and elevated glycated hemoglobin with associated increase in complication rates in diabetes patients. However, the role of periodontal infection in beta cell dysfunction is not known, however.

Clinical consequences of reduced glycated hemoglobin in response to treating periodontal infection are yet to be determined. It is possible, however, that treating periodontal infection in patients with diabetes will reduce systemic TNF-alpha and other mediators derived from infected periodontal tissues and, thus, reduce the systemic effects of periodontal infections. Hence, treating periodontal disease may modulate, in some part, factors associated with increased insulin resistance. Studies are needed to assess the mechanisms involved in this two-way relationship with diabetes mellitus increasing the risk for periodontal disease, and periodontal infections increasing or resulting in poor glycemic control. In addition, large prospective, randomized controlled trials are warranted to determine the effects of periodontal therapy on glycemic control and important complications of diabetes including cardiovascular disease, nephropathy, and retinopathy. The public health implications of these studies are potentially important because periodontal disease and diabetes mellitus are common chronic diseases.

References:

1. Nelson RG, Shlossman M, Budding LM, Pettitt DJ, Saad MF, Genco RJ, Knowler WC. Periodontal disease and non-insulin-dependent diabetes mellitus in Pima Indians. Diabetes Care 1990;13:836–840.

2. Emrich LJ, Shlossman M, Genco RJ. Periodontal disease in non-insulin-dependent diabetes mellitus. J Periodontol 1991;62:123–130.

3. 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;104:653–660.

4. Taylor GW, Burt BA, Becker MP, Genco RJ, Shlossman M, Knowler WC, Pettitt DJ. Severe periodontitis and risk for poor glycemic control in subjects with non-insulin-dependent diabetes mellitus. J Periodontol 1996;67(Suppl):1085–1093.

5. Grossi SG, Skrepcinski FB, DeCaro T, Zambon JJ, Cummins D, Genco RJ. Response to periodontal therapy in diabetics and smokers. J Periodontol 1996;67(Suppl):1094–1102.

6. Schmidt AM, Weidman E, Lalla E, et al. Advanced glycation endproducts (AGEs) induce oxidant stress in the gingiva: A potential mechanism underlying accelerated periodontal disease associated with diabetes. J Periodontal Res 1996;31:508–515.

7. Lee TS, Saltsman KA, Ohashi H, King GL. Activation of protein kinase C by elevation of glucose concentration: Proposal for a mechanism in the development of diabetic vascular complications. Proc Natl Acad Sci (USA) 1989;86:5141–5145.

8. Kanety H, Feinstein R, Papa MZ, Hemi R, Karasik A. Tumor necrosis factor alpha-induced phosphorylation of insulin receptor substrate-1 (IRS-1). Possible mechanism of suppression of insulin-stimulated tyrosine phosphorylation of IRS-1. J Biol Chem 1995;270:23780–23784.

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Page last reviewed: February 2, 2005
Content source: Division of Oral Health, National Center for Chronic Disease Prevention and Health Promotion