Association between periodontitis and hyperlipidemia: Cause or effect?

Background: Epidemiological studies suggest a relationship between periodon titis and coronary artery disease, but the mechanism has not been establish ed. Recent studies in animals indicate that low dose endotoxin, as in a Gra m-negative infection, can induce hyperlipidemia and myeloid cell hyperactiv ity. The association between periodontitis, systemic exposure to Porphyromo nas gingivalis, lipopolysaccharides (LPS), and hyperlipidemia has not been examined in humans. Methods: Sera were obtained from 26 adult periodontitis patients and 25 hea lthy control (C) subjects selected from patients and staff. Serum antibodie s against Porphyromonas gingivalis and its LPS were analyzed by enzyme-link ed immunosorbent assay (ELISA) and Western blotting, respectively. Serum tr iglycerides (TG) and cholesterol (CHOL) were assayed by a commercial labora tory. The associations between AP and blood levels of TG, CHOL, and anti-P. gingivalis whole cells and LPS were examined by logistic regression analys is. Peripheral blood polymorphonuclear leukocytes (PMNs) from 6 healthy fas ted donors were incubated with purified TG (0.1 mg/ml) for 2 hours at 37 de grees C, stimulated with 100 ng/ml P. gingivalis LPS, and the release of IL -1 beta measured by ELISA. Results: The presence of periodontitis was significantly associated with ag e (odds ratio = 3.5, P = 0.04), elevated TG levels (odds ratio = 8.6, P = 0 .0009), elevated CHOL levels (odds ratio = 7, P = 0.004), elevated ELISA ti ter (odds ratio = 35, P = 0.003) and reactivity with P. gingivalis LPS (odd s ratio = 41, P = 0.001). PMNs from all 6 healthy patients released modest levels of IL-1 beta (10 to 60 pg/ml) when stimulated with 100 ng/ml P. ging ivalis LPS. Addition of TG resulted in a significant increase (P < 0.05) in IL-1 beta secreted that ranged from 7 to 150% over LPS alone. No IL-1 beta was elicited by TG or vehicle alone. Conclusions: The results of this study indicate the presence of a significa nt relationship between periodontitis, hyperlipidemia, and serum antibodies against P. gingivalis LPS that warrants further examination in a larger pa tient population. Furthermore, these studies indicate that elevated triglyc erides are able to modulate IL-1 beta production by PMNs stimulated with P. gingivalis LPS.