ABSTRACT
Although periodontal disease may be associated with increased risk for atherosclerosis, the mechanism by which the disease causes atherosclerosis is still unknown. The candidates contributing to atherosclerosis in periodontal disease include low-grade inflammation such as C-reactive protein (CRP) and insulin resistance. A previous study demonstrated that periodontal therapy leads to an improvement in CRP as well as insulin resistance, indicating the relationship between periodontal disease and low-grade inflammation or insulin resistance. On the other hand, we previously demonstrated that serum triglyceride (TG) per se is independently associated with CRP or insulin resistance in Japanese populations with a body mass index (BMI) of 21.5 to 27.0 (midrange BMI). To the best of our knowledge, however, the relationship between periodontal disease and serum TG is not fully clarified. The first aim of the present study is to investigate whether periodontal disease is associated with serum TG in Japanese subjects with midrange BMI. If so, another aim of the study is to determine which mechanism is responsible for the association between periodontal disease and serum TG in these subjects. We have performed a periodontal examination in the Ogaki metabolic syndrome medical examination. One hundred sixty-two participants from 40 to 74 years old (56 men and 106 women; mean age, 66.43 ± 6.25 years) were enrolled in the study. Besides medical examination, oral panoramic radiograph was taken for all participants. Average bone score was also calculated. Periodontal bone destruction increased according to the age of the participants (r = 0.227, P < .004, Spearman correlation coefficient). Periodontal bone destruction was also associated with serum TG levels (r = 0.299, P = .000). This association was more evident in subjects with midrange BMI (r = 0.332, P < .001). In subjects with midrange BMI, TG was not correlated with BMI or waste circumstances. Furthermore, TG was not associated with age itself in the midrange BMI group. We then investigated the lipolytic activity of endotoxin in cocultures of adipocytes and macrophages. Low-dose lipopolysaccharide dose-dependently increased lipolytic activity in cocultures, and this activity was neutralized by anti-tumor necrosis factor α neutralizing antibodies. These results suggest that periodontal infection, especially bacterial endotoxinemia, is associated with enhanced lipolysis and subsequent up-regulation of circulating TG in Japanese with midrange BMI.
