Coronary heart disease (CHD) is the leading cause of death among patients with type 2 diabetes. Several factors were observed to be associated with an increased risk of major manifestations of CHD. Elevated levels of C-reactive protein (CRP), although often in the healthy reference range, have been associated with increased risk of future CHD (1). We hypothesized that periodontal infection might contribute to the elevated CRP in diabetic populations, since periodontal disease has recently been declared the sixth complication of diabetes (2). Serum IgG antibody levels against several periodontal pathogens, especially against Porphyromonas gingivalis (P. gingivalis), are elevated in chronic adult periodontitis patients and decline with therapy (3). However, a major problem is that the degree of being overweight or of hyperglycemia per se greatly affects CRP levels in type 2 diabetes. To overcome this difficulty, we recruited nonobese well-controlled unique Japanese type 2 diabetic patients who had no evidence of cardiovascular disease, ischemic stroke, hepatic disorders, or chronic renal failure and investigated the association between IgG titer against P. gingivalis and CRP level. A total of 131 patients aged 36–84 years were enrolled in the study. The patients were nonobese (BMI >20.0 and <27.0 kg/m2) and were well controlled in terms of HbA1c (mean HbA1c 7.2%) and blood pressure (BP) (mean BP 130/76 mmHg). All diabetic subjects were treated either with sulfonylureas or with diet alone. None of them received insulin therapy.

No significant correlation was observed between high sensitive CRP value and known risk factors such as triglycerides (r = 0.108, P = 0.108; Spearman’s correlation coefficiency), LDL cholesterol (r = 0.155, P = 0.155), hyperglycemia (FBS r = 0.125, P = 0.156; HbA1cr = 0.153, P = 0.152), and the degree of obesity (BMI) (r = 0.161, P = 0.161), except for a very weak correlation with total cholesterol (r = 0.047, P = 0.047). Yet, significant correlations between high sensitive CRP value and IgG titers against P. gingivalis FDC 381 (serotype a) and against SU63 (serotype b) were observed (r = 0.219, P < 0.013 and r = 0.233, P < 0.008, respectively). Serum IgG titer to P. gingivalis, however, did not correlate with lipid abnormalities.

Thus, it is possible that periodontal infection is an independent contributing factor for future cardiovascular events, as recently proposed by others (4). However, there is another possibility that elevated CRP is simply a result of local periodontal infection. In that case, high sensitive CRP may not be a good marker to predict cardiovascular risk. Therefore, we need to undertake a large epidemiological study investigating the relationship between chronic periodontitis and cardiovascular events in such nonobese well-controlled patient populations.

This work was supported by a grant-in-aid from the Japan Society for the Promotion of Science (nos. 13307055, 13357018, and 14657555).

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Address correspondence to Fusanori Nishimura, Department of Pathophysiology/Periodontal Science, Okayama University Graduate School of Medicine and Dentistry, 2-5-1 Shikata-cho, Okayama 700-8525, Japan. E-mail: fusanori@md.okayama-u.ac.jp.