OBJECTIVETo make an animal periodontitis and atherosclerosis compound model, and to study the effects of periodontitis on atherosclerosis.

METHODS36 Japan rabbits were randomly divided into four groups: Including periodontitis model group, periodontitis and atherosclerosis compound model group, atherosclerosis model group and control group. Periodontitis model was initiated by ligating floss around teeth cervical and oral inoculating with Porphyromonas gingivalis (P. gingivalis). Atherosclerosis was established by single iliac artery of balloon-injured rabbit. Histopathological change of injured iliac artery was observed under optical microscope after hematoxylin-eosion stain. Elastica van Gieson-stained sections were used for the morphometric analysis. We measured intimal and medial lesion areas in iliac artery cross-sections as well as the intimal/medial ratio (I/M). We also analyzed P. gingivalis 16S rDNA amplification with nested-polymerase chain reaction (nested-PCR), and detect systemic proinflammatory mediators with enzyme linked immunosorbent assay (ELISA), including C-reactive protein (CRP), interleukin-6 (IL-6) and interleukin-1beta (IL-1beta).

RESULTSThe serum levels of CRP, IL-6 and IL-1beta increased obviously among the compound model group than other groups (P<0.01). Histopathological observation revealed the compound model group in I/M was bigger than other groups (P<0.01). P. gingivalis 16S rDNA was detected among the periodontitis model group and the compound model group by nested-PCR.

CONCLUSIONPeriodontitis may accelerate intimal hyperplasia in balloon-injured iliac arteries by upgrade of systemic inflammation factors and local bacterial infection.