INTRODUCTION

Definitions

The characteristic metabolic disorder in diabetes is hyperglycemia. Diabetes mellitus is characterized by chronic elevated levels of glucose in the blood. The diagnosis of diabetes is made with fasting plasma glucose levels of 126 mg/dL or greater. Diabetes mellitus results from a dysregulation of glucose metabolism due to the decreased production of insulin by the β cells of islets of Langerhans in the pancreas.

Diabetes is a chronic disease of adults and children and is of two types:

High levels of glycosylated hemoglobin (HbA1c) are the result of elevated blood glucose levels over a period of a few months before the day of blood analysis. HbA1c is a good measure of long-term glucose levels. The normal serum levels of glycosylated hemoglobin are between 4% and 6% (Ship 2003). Severely elevated levels are greater than 9%, and mildly elevated levels are between 7% and 9% (Madden et al. 2008).

Glycemic control is based on following factors:

• better nutrition
• weight loss
• self-monitoring of blood glucose levels
• prevention and treatment of infections (Madden et al. 2008)

Complications

Poorly controlled blood glucose level is the principal cause of vascular complications. There are two types of cardiovascular complications in diabetes:

Diabetic microangiopathy is responsible for compromised delivery of nutrients to tissues and poor elimination of metabolic products. Diabetes induces most of its complications on blood vessels, on large vessels with macroangiopathy, and on small vessels with microangiopathy.

Uncontrolled diabetes with poor glycemic control is a risk factor for severe periodontitis. The treatment of periodontitis improves glycemic control (Boehm and Scannapieco 2007). Mean advanced alveolar bone loss is significantly associated with eye vascular complication or retinopathy, with an odds ratio of 8.86 (Negishi et al. 2004). Porphyromonas gingivalis is capable of invading endothelial cells causing vascular damage; infection worsens glycemic control inducing hyperglycemia and increases the severity of microvascular and macrovascular pathology (Grossi et al. 2001).

Patient Management

Periodontitis may influence the severity of diabetes because of inflammation and uncontrolled glucose levels, and treatment of periodontal disease may be beneficial to diabetes control. Health education to encourage better oral care is necessary to reduce the prevalence of the diabetic disease and its complications.

For dentists, knowledge of the general and oral signs of diabetes are necessary. Dentists must be prepared to manage diabetic emergencies:

• low blood glucose levels or hypoglycemia (the most frequent complication)
• high blood glucose levels or hyperglycemia, with possible ketoacidosis or coma.

Dentists should be aware of circumstances that can induce hyperglycemia, such as infections, corticosteroids, surgery, stress, and medications, or circumstances that can induce hypoglycemia, such as an inappropriate diet or treatment and associated medications (Ship 2003).

Diabetes care should include personal glucose monitoring with blood tests. Regular care should also include laboratory information regarding levels of blood glucose, glycosylated hemoglobin for glycemic control, leukocyte count for infections, C-reactive protein for inflammation, and creatinine for renal failure. Before any oral procedure, fasting glucose and glycosylated hemoglobin must be checked (Taylor 2003).

In case of surgery, antibiotic therapy may be used to prevent or treat oral infections, because opportunistic infections are more frequent with uncontrolled diabetes.

Endodontic and periodontic lesions of teeth are associated with hyperglycemia and may necessitate a sudden increase in insulin demand in order to normalize glucose levels. But after dental and periodontal treatment, the insulin need returns to baseline (Schulze, Schonauer, and Busse 2007).

Diabetes and Periodontitis

Periodontitis is twice as prevalent in diabetic patients than in healthy subjects (Grossi et al. 2001). Diabetes is a modifying and aggravating factor in the severity of periodontal disease. Periodontitis results from an interplay of bacterial infection and host response. Severe periodontitis often coexists with diabetes mellitus; periodontitis increases the severity of diabetes and complicates metabolic control. Infection and advanced glycation end products–mediated cytokine response is responsible for periodontal tissue destruction. The host response to infection is an important factor in extension and severity of periodontal disease; periodontitis severity and prevalence are increased in diabetes. Diabetes and periodontitis can both stimulate chronic production of inflammatory cytokines. These cytokines are elevated in periodontitis and may in turn predispose to diabetes. Cytokines can promote insulin resistance and cause the destruction of pancreatic beta cells, inducing diabetes (Duarte et al. 2007; Grossi 2001; Iacopino 2001; Kuroe et al. 2006; Nassar, Kantarci, and van Dyke 2000; Nibali et al. 2007; Nishimura et al. 2003; Novak et al. 2008). Oral diseases are associated with diabetes. Periodontitis is a risk factor for poor glycemic control and complications of diabetes. Sometimes periodontitis may be the first clinical manifestation of diabetes (Lamster, Lalla, and Borgnakke 2008). Periodontal indices, such as probing depth, attachment loss, and tooth loss, are significantly higher in diabetes family members (Meng 2007). There is a significant association between diabetes and deep probing depths and severe alveolar bone loss (Negishi et al. 2004). Periodontal infection is responsible for chronic inflammation, periodontal tissue destruction, and impaired tissue repair (Iacopino 2001).

Periodontal Therapy

Successful anti-infectious periodontal therapy has a beneficial effect on metabolic control of type 2 diabetes and glucose regulation. Proinflammatory cytokines, such as tumor necrosis factor-α (TNF-α), produced from excess amount of adipocytes, are responsible for lowered insulin sensi­tivity, called insulin resistance, and hyperglycemia. Diabetes can affect the periodontal tissues and the treatment of periodontal disease. Successful antimicrobial periodontal therapy may then result in improved insulin resistance and better glycemic control (Grossi et al. 1997; Katz 2005; Lalla, Kaplan et al. 2007; Madden 2008; Navarro-Sanchez, Faria-Almeida, and Bascones-Martinez 2007; O Connell 2008). Diabetes and periodontitis are secondary to chronic inflammation, altered host response, or insulin resistance. Periodontitis is associated with an elevated systemic inflammatory state and increased risk of hyperglycemia. Periodontal therapy that causes the decrease of oral bacterial load and reduction of periodontal and systemic inflammation can improve blood glucose control (Mealey and Rose 2008).

TYPE 2 DIABETES MELLITUS

Periodontal Treatment

Preventive periodontal therapy should be intense enough to reduce periodontal inflammation and glycosylated hemoglobin levels. Periodontitis treatment should include scaling, root planing, oral hygiene instruction, and chlorexidine rinse treatment (Madden et al. 2008). After nonsurgical periodontal therapy, significant probing depth reduction is observed after full-mouth scaling and root planing, with improvement in glycemic control and reduction in glycated hemoglobin levels (Rodrigues, Taba, and Novaes 2003). After full-mouth subgingival debridement in diabetic patients, many subgingival bacterial species are reduced, such as P. gingivalis, Tannerella forsythensis, Treponema denticola, and Prevotella intermedia. P. gingivalis is detected more frequently in patients with increased glycosylated hemoglobin levels and worse glycemic control (Makiura et al. 2008). After periodontal therapy, including scaling, root planing, and doxycycline, there is a significant reduction of 1.1 mm in probing depth, a reduction of 1.5% in glycosylated hemoglobin levels, and reduction in serum inflammatory mediators such interleukin-6 (IL-6) and granulocyte colony-stimulating factor (O’Connell/>