The Oral-Medical Disease Connection: Diabetes

[DrAnil]

Periodontal Disease and Diabetes

It is estimated that diabetes affects 20 million Americans, while 35% to 40% of Americans have not received a diagnosis. Currently, more than 9% of the US adult population has diabetes, and this number is expected to grow significantly in the future. The two main types of diabetes are classified primarily on the basis of their underlying pathophysiology. Type 1 diabetes, which constitutes about 5% to 10% of all cases in the United States, results from autoimmune destruction of insulin-producing beta cells in the pancreas, leading to total loss of insulin secretion. Insulin is used by the body to facilitate the transfer of glucose from the blood stream into target tissues such as muscle where glucose is used for energy. Since a person with Type 1 diabetes no longer produces endogenous insulin, glucose is unable to enter target cells and remains in the blood stream, resulting in sustained hyperglycemia. A patient with Type 1 diabetes, therefore, must take exogenous insulin to remain alive, hence, the former name “insulin-dependent diabetes.”

Type 2 diabetes constitutes about 85% to 90% of all diabetic cases and results from insulin resistance rather than from a total absence of insulin production. Autoimmune destruction of beta cells does not occur in these patients, and they do retain the capacity to secrete some insulin; although, production often diminishes over time. Type 2 diabetes patients remain undiagnosed for many years because hyperglycemia appears gradually and often without symptoms. Insulin resistance results in a decreased capacity to transfer glucose into target cells, resulting in hyperglycemia.

The relationship between diabetes and periodontal disease has been the subject of more than 200 articles published in English over the past 50 years. Interpretation of this research is made difficult by the numerous classifications for diabetes and periodontitis used over the years. Varying clinical and radiographic criteria used to assess periodontal disease and the extent and severity of the disease also make it challenging to establish relationships. In addition, evolving standards for the degree of glycemic control and changing methodology for assessing the complications associated with diabetes have made interpretation of the research difficult at best. Most of the research has focused on assorted populations and often has included relatively few subjects or has lacked controls. Evidence suggesting diabetes as a risk factor for gingivitis and periodontitis dates back to the 1950s. Increased gingival inflammation is seen in children with Type 1 diabetes, as is the greatest severity of gingivitis in patients with very poor glycemic control. Evidence suggests that diabetes mellitus increases the risk of developing periodontitis. Lalla has documented increased prevalence and severity of attachment loss in adults and children with diabetes, and there is increased loss with poor glycemic control. There appears, however, to be significant individual variability in the degree to which glycemic control influences periodontal status. How diabetes affects gum disease and how gum disease affects the metabolic state seem to be evolving narratives. Intervention trials have resulted in varied metabolic responses in patients with diabetes mellitus. A meta-analysis of 10 intervention trials (> 450 patients) found an average decrease in absolute hemoglobin HbA1c values of 0.4% after scaling and root planing.⁶¹ The addition of systemic antibiotic therapy resulted in mean absolute reduction of HbA1c of 0.7%; although, not statistically significant, clinical significance in the practice of medicine is defined by a change of 0.6%. The mechanism of interaction between diabetes and periodontal disease focuses on the function of cells, including altered neutrophil, monocyte, and macrophage function. In addition, there is up regulation of other immunoregulatory responses, including IL-1b and TNF-α. The altered wound healing that is seen in diabetes relates to poor fibroblast function in a high glucose environment. In addition, there is elevation of MMPs. In diabetes, changes in microvascular integrity lead to end-organ damage, which includes the presence of advanced glycosylated end-products in the periodontium. Inflammation is a common theme in both Type 1 and Type 2 diabetes, as is periodontal disease. Inflammation is a known cause of insulin resistance. Chronic periodontal disease can, therefore, increase insulin resistance and worsen glycemic control. This can happen secondarily as periodontal disease increases pro-inflammatory cytokines, which can lead to insulin resistance. Currently, commercially available salivary diagnostic tests attempt to identify the type and concentration of specific pathogenic bacteria known to cause periodontal disease. In addition, other tests claim to identify individual genetic susceptibility to periodontal disease to enable the clinician to establish which patients are at increased risk for more severe periodontal infection due to an exaggerated immune response. Those recommended to be tested include patients who have a family history of diabetes.

 

 

Although there is no conclusive evidence that treating oral disease will prevent heart attack, stroke, diabetes, or adverse pregnancy outcomes, dental professionals should promote a message that a strong biologic connection exists between oral and systemic health. Emergence of this topic and new data is leading to a convergence in oral and medical care that clearly benefits public health.