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Experimental Periodontitis Induces Inflammatory Gene Expression in the Aorta

T. DESTA, Q. LUAN, P. KROTHAPALLI, and D.T. GRAVES, Boston University, MA, USA

It is thought that periodontal disease may aggravate cardiovascular disease by enhancing systemic inflammation.

Objective: the goal of this study was to investigate whether experimental periodontitis induced an inflammatory response that could be detected both locally and in cardiovascular tissue.

Methods: Ligatures were placed around second molar of rats to induce experimental periodontitis and left in place for seven days. Three groups of animals were tested: No ligature (baseline), ligature placement for 7 days and 4 days after ligature removal to examine resolution of inflammation. RNA was extracted from the aorta and gingival tissue by RNAeasy MiniPrep and mRNA levels were examined by quantitative real-time PCR using primers and probe sets from Applied Biosystems. Significance was established by one way analysis of variance (ANOVA).

Results: Seven days after ligature were placed the aorta showed a 2 fold increase in TNF-á, 3 fold increase in VCAM-1, 8 fold increase in ICAM-1, and 6 fold increase in IL-6 compared to baseline. All values were significant (P<0.05). The level of TNF-á and VCAM-1 returned to baseline four days after removal of ligatures (P>0.05) while ICAM-1 and IL-6 remained elevated 3 fold compared to the baseline (P<0.05). In the gingiva, both TNF-á and VCAM-1 were elevated by 2 fold in the seven day groups (P<0.05). Both genes remained elevated four days after ligatures were removed (P<0.05). Enhanced IL-6 expression was elevated 2 fold in the four-day after ligature removal group (P<0.05).

Conclusion: The onset of experimental periodontitis causes the induction of inflammatory genes locally and in the aorta demonstrating that conditions that cause local inflammation in the gingiva affect cardiovascular tissue.

Seq #237 - Periodontal -Systemic Interactions
3:30 PM-4:45 PM, Friday, March 23, 2007 Ernest N. Morial Convention Center Exhibit Hall I2-J

 

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