Diabetes And Periodontal Disease

Diabetes And Periodontal Disease

Mechanism of Influence of Diabetes on Progression of Periodontitis

The risk of developing destructive peiodontitis increase threefold in diabetic individuals. Following are the various mechanisms which lead to the progression of periodontal therapy on diabetics:

Alteration in Bacterial Pathogens

• The glucose content in the blood and gingival fluid of individuals with diabetes could change the environment of the microflora, inducing qualitative changes in bacteria that could account for the severity of periodontal disease observed in poorly controlled individuals with diabetes.
• There is altered flora in the periodontal pockets of patients with diabetes.
• Patients with type 1 diabetes with periodontitis have been reported to have a subgingival flora composed mainly of Capnocytophaga, anaerobic vibrio and Actinomyces species.
• P. gingivalis, P. intermedia and C. rectus are more prominent in Type 2 diabetics.

Polymorphonuclear Leucocyte Function

• The increased susceptibility of diabetics to infection has been hypothesized as being due to polymorphonuclear leucocyte deficiencies resulting in impaired chemotaxis, defective phagocytosis, or impaired adherence.
• In patients with poorly controlled diabetes the function of PMN leucocytes and monocytes/macrophages is impaired.
• No alteration of IgA, IgG or IgM has been found in diabetics.

Altered Collagen Metabolism

• Increased collagenase activity and decreased collagen synthesis is seen in individuals with diabetes with chronic hyperglycemia.
• Chronic hyperglycemia adversely affects the synthesis, maturation and maintenance of collagen, and extracellular matrix molecules undergo a non-enzymatic glycosylation, resulting in advanced glycation end products (AGEs).
• The formation of AGEs can occur at normal glucose levels, but in hyperglycemic environments, AGE formation is excessive. AGE formation crosslinks collagen, making it less soluble and less likely to be normally repaired or replaced. As a result, collagen in the tissues of poorly controlled diabetics is aged and more susceptible to breakdown.
• AGEs play a central role in the classic complications of diabetes. They may play a significant role in the progression of periodontal disease as well.
• Poor glycemic control and increased AGEs render the periodontal tissues more susceptible to destruction.
• Cellular migration through crosslinked collagen is impeded and perhaps more importantly, tissue integrity is impaired as a result of damaged collagen remaining in the tissues for longer periods.

Influence of Periodontal Therapy in Glycemic Control

• Acute bacterial and viral infections have been shown to increase insulin resistance and aggravate glycemic control. This occurs in individuals with and without diabetes.
• Systemic infections increase tissue resistance to insulin, preventing glucose from entering target cells, causing elevated blood glucose levels, and requiring increased pancreatic insulin production to maintain normoglycemia. Insulin resistance may persist for weeks or even months after the patient has recovered clinically from their illness.
• In the individual with type 2 diabetes, who already has significant insulin resistance, further tissue resistance to insulin induced by infection may considerably exacerbate poor glycemic control.
• In type l patients, normal insulin doses may be inadequate to maintain good glycemic control in the presence of infection-induced tissue resistance. It is possible that chronic gram-negative periodontal infections may also result in increased insulin resistance and poor glycemic control.
• In patients with periodontitis, persistent systemic challenge with periodontopathic bacteria and their products may act similar to well-recognized systemic infections. This mechanism would explain the worsening of glycemic control associated with severe periodontitis. Periodontal treatment designed to decrease the bacterial insult and reduce inflammation might restore insulin sensitivity over time, resulting in improved metabolic control. The improved glycemic control seen in several studies of periodontal therapy would support such a hypothesis.