| Objective:To investigate the influence of the chronic infection of P. g to carotid atherosclerotic plaque in SD rats.Methods:70SD rats were selected to conduct the investigation.10rats were killed at the very beginning(designated as TO). The rest60SD rats were divided into2groups randomly:including periodontitis model group and control group. Peridontitis model was initiated by ligating floss around teeth cervical and inoculating P. g. Histopathological change of carotid artery was observed under optical microscope after hematoxylin-eosion(HE) stain. We measured intimal and medial lesion areas in carotid artery cross-sections as well as the intimal/medial ratio (I/M) in different time(differently designated as TO, Tl, T2,T3). Nested-polymerase chain reaction (nested-PCR) was adopted to analyze P. gingivalis16S rDNA amplification. Serum lipid was as well observed during different periods.Result:It revealed in histopathological observation that the I/M in periodontitis model group was distinctly bigger than that in the control group (P<0.05). P. g16S rDNA was detected in carotid artery (T2ã€T3) and blood (T1,T2, T3) among the periodontitis model group by nested-PCR. The serum lipid in periodontitis model group is higher than that in the control group.Conclusion:the:the chronic infection of Pg. may accelerate the progress of carotid atherosclerotic plaque in SD rats. |