Periodontitis and diabetes

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Abstract

Periodontitis and diabetes are complex chronic diseases, linked by an established bidirectional relationship. Risk for periodontitis is increased two to three times in people with diabetes compared to individuals without, and the level of glycaemic control is key in determining risk. In people who do not have diabetes, periodontitis is associated with higher glycated haemoglobin (HbA1c) and fasting blood glucose levels, and severe periodontitis is associated with increased risk of developing diabetes. In people with type 2 diabetes, periodontitis is associated with higher HbA1c levels and worse diabetes complications. Treatment of periodontitis in people with diabetes has been shown to result in improved glycaemic control, with HbA1c reductions of 3-4 mmol/mol (0.3-0.4%) in the short term (3-4 months) post-treatment. Given that treatment of periodontitis results in clinically relevant reductions in HbA1c, the dental team has an important role in the management of patients with diabetes. Improved interprofessional working in relation to diabetes and periodontitis has been advocated by professional and scientific organisations, though practical and systemic barriers make this challenging. This paper reviews current evidence linking periodontitis and diabetes, and considers the role of the dental team in the wider context of management of patients with diabetes and periodontitis.

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A systematic review and meta-analyses on C-reactive protein in relation to periodontitis.

Spiros Paraskevas, John D Huizinga, Bruno Loos (2008)

Elevated plasma C-reactive protein (CRP) is regarded as a risk predictor for cardiovascular diseases. This systematic review explored the robustness of observations that CRP is elevated in periodontitis. Similarly, the effect of periodontal therapy on CRP levels was investigated. Selection of publications was based on: (1) cross-sectional (case-control) studies; (2) longitudinal (treatment) studies; (3) high-sensitivity CRP measurement; (4) median and/or mean (+/-SD) values presented; and (5) subjects with no systemic disorders. Screening of the initially 448 identified studies and reference checking resulted in 18 suitable papers. The majority of the studies showed that CRP levels are higher in patients than in controls. Often, studies showed that patients had CRP levels >2.1 mg/l. A meta-analysis of 10 cross-sectional studies showed that the weighted mean difference (WMD) of CRP between patients and controls was 1.56 mg/l (p<0.00001). Evidence from available treatment studies (n=6) showed lower levels of CRP after periodontal therapy. Eligible treatment studies in a meta-analysis demonstrated a WMD of reductions of CRP after therapy of 0.50 mg/L (95% CI 0.08-0.93) (p=0.02). There is strong evidence from cross-sectional studies that plasma CRP in periodontitis is elevated compared with controls. There is modest evidence on the effect of periodontal therapy in lowering the levels of CRP.

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Systemic markers of inflammation in periodontitis.

Bruno Loos (2005)

This literature review summarizes current knowledge on the systemic levels of selected markers of inflammation in periodontitis. From samples of peripheral blood the following cellular factors are discussed: total number of white blood cells, red blood cells, and thrombocytes. Further, plasma levels of acute-phase proteins, cytokines, and coagulation factors are reviewed. From the available literature it appears that the total numbers of leukocytes and plasma levels of C-reactive protein are consistently higher in periodontitis patients compared to healthy controls. Numbers of red blood cells and levels of hemoglobin are lower in periodontitis and there is a trend towards anemia of chronic disease. Most systemic markers of inflammation discussed in this review are also regarded as predictive markers for cardiovascular diseases. Therefore, changes in these markers in periodontitis may be part of the explanation why periodontitis is associated with cardiovascular diseases and/or cerebrovascular events in epidemiological studies. It is hypothesized that possibly daily episodes of a bacteremia originating from periodontal lesions are the cause for the changes in systemic markers in periodontitis; the cumulative size of all periodontal lesions in the untreated severe patient may amount to 15 to 20 cm2.