Pathological Study on Atherosclerosis Experimentally Induced by Enterococcus faecalis in Rat
DOI:
https://doi.org/10.22317/imj.v9i1.1305Keywords:
Enterococcus faecalis, Oxidative Stress, Vegetative Endocarditis, AtherosclerosisAbstract
Objectives
This study aimed to investigate the potential role of Enterococcus faecalis in the development of atherosclerosis, focusing on two primary mechanisms: the induction of vegetative endocarditis and the promotion of oxidative stress. By examining systemic effects following dissemination of E. faecalis, commonly associated with dental infections, the study sought to explore its possible contribution to cardiovascular pathology.
Methods
E. faecalis was isolated from dental caries lesions and identified as gram-positive cocci using selective and differential culture media. Twenty adult albino rats were randomly divided into two groups (n=10 per group). Group 1 served as the control, while Group 2 received an intraperitoneal injection of E. faecalis suspension (1 mL, 7.8 × 10⁷ CFU/mL). After 90 days, oxidative stress biomarkers—GSH, SOD, TAC, MDA, NO, IL-6, and TNF-α—were measured in cardiac and aortic tissues. Serum CRP levels were assessed to evaluate systemic inflammation. Histopathological examinations of the aorta and heart were conducted to assess structural and inflammatory changes.
Results
Infected rats exhibited significant histopathological alterations in the aorta, including lipid vacuole accumulation, foam cell infiltration in intima and media layers, and fragmentation of elastic fibers. Cardiac examination revealed vegetative endocarditis with bacterial colonies, mononuclear cell infiltration, myocardial fatty degeneration, and mural valve thrombi. Coronary arteries displayed wall thickening, thrombus formation, and periarteritis. Biochemical assays showed elevated oxidative stress markers and significantly increased CRP levels in Group 2 compared to controls.
Conclusion
The findings suggest that systemic E. faecalis infection can contribute to atherosclerosis by promoting both vegetative endocarditis and oxidative stress. This supports a mechanistic link between oral bacterial infections and cardiovascular disease, underscoring the importance of oral health in systemic disease prevention.
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