This study aimed to determine whether coffee consumption affects the structure of coronary arterial wall and protects against coronary artery disease (CAD) in atherosclerotic rat model induced by periodontitis. Rats (n=21) were divided into three groups (i) Coffee group (periodontitis + coffee), (ii) Periodontitis group (no coffee), and (iii) Control group (no periodontitis, no coffee). A single dose of coffee suspension (representing one cup) was given daily by stomach sondation to the rats in the coffee group. The experiment was conducted for 5 wk. At the completion of the experiment, all of rats were sacrificed. Their hearts containing coronary arteries were removed and analyzed by histochemistry assay. In addition, the serum level of collagen degrading enzymes matrix metalloproteinase-2 (MMP-2) was also analyzed using Enzyme-link immunosorbent assay (Elisa). Results demonstrated that coronary atherosclerotic lesions including atheroma, stenosis, and vascular occlusion were rarely identified in the coffee group. The coronary arterial wall demonstrated relatively symmetrical intima-media thickness (IMT) and the lumen diameter remained adequate for blood flow. The intimal collagen was intact, dense and thick. MMP-2 level was significantly lower (P < 0.05) in the coffee group. In conclusion, coffee maintained the structure of coronary arterial wall particularly the intimal collagen, providing protection against CAD. This might also mediate the vascular resistance against rupture and thrombosis that might precipitate the occurrence of acute coronary syndrome (ACS).
Context: Epidemiological and microbiological studies have reported association between periodontitis and coronary artery disease (CAD), experimental study that simulated cause-effect of periodontitis in CAD, however, was lacking. Aims: This study aimed to demonstrate the occurrence of coronary artery disease as a consequence of induced periodontitis in a rat model. Settings and Design: This in vivo experimental study using the post test only control group design. Methods and Material: A total of 12 rats (Rattus norvegicus) were divided into control and periodontitis groups (six rats in each group). Periodontitis was induced by injection of periodontitis bacteria Porphyromonas gingivalis in buccal gingival sulcus of left mandibular teeth, thrice a week for 4 wk. All rats were fed with normocholesterol diet. At the end of study, all rats were sacrificed. The rats'heart containing coronary arteries were removed, cut cross-sectionally and prepared for histochemistry assay. Statistical analysis used: Descriptive analysis was used to assess the frequency of CAD lesion, and t test for IMT Results: All of rats in periodontitis group demonstrated signs of CAD. Coronary artery local inflammation indicated by leukocytes and erythrocyte accumulation were identified in all rats in periodontitis group (100 %). Parameters of intimal collagen disintegration and endotelial disintegration were also commonly occured (91.66 % each), atheroma (41.66 %), stenosis (41.66 %). Periodontis group demonstrated significantly higher mean IMT (p < 0.05) compared to control group, 3.6 µm ± 1.4 µm and 2.1 µm ± 0.7 µm, respectively. Conclusions: Periodontitis induced CAD. Periodontitis rat model might be used to represent as atherosclerotic model as well..
Stimulated neutrophil is the main source of oxidants/free radicals, that might contribute to the state of oxidative stress. Coffee has been well known to have a high antioxidant capacity, therefore it was plausible to hypothesize that coffee might reduce oxidants/radicals produced by neutrophil. This study aimed to analyze effect of coffee on superoxide radical produced by neutrophil in vitro. This study was conducted experimentally using the post test only control group design. Neutrophil was isolated from healthy human peripheral blood. Superoxide radical production was analyzed by NBT (nitro blue tetrazolium) assay. Results showed that coffee significantly (P < 0.05) reduced the number of neutrophils that produce superoxide radicals. In conclusion, coffee demonstrated antioxidant capacity against neutrophil superoxide radicals.
Cardiovascular disease is the most deadly disease in the world and the main cause is atherosclerosis. New paradigm explains that chronic inflammation such as periodontitis is considered to be a risk factor for atherosclerosis. Periodontitis causes bacteremia affecting vascular inflammation. This situation affects the endothelial cells and lipid oxidation thereby increasing the risk of atherosclerosis. This study aimed to prove the effect of periodontitis on coronary atherosclerotic lesion formation. Methods: This was an experimental study using the post-test only control group design. Samples were 12 rats divided into control group (K) without treatment and periodontitis (P) was made with the installation of wire ligature and injection of Porphyromonas gingivalis on the left mandibular M1 for 28 days. On day 29, mice were decaputated, coronary artery was taken and histological slides were made. Histomorphometrical analysis was calculated on dungkul (descriptive) and the thickness of the arterial wall (with test statistic T test). Results: The results showed higher formation of arterial dungkul on Periodontitis group (83.33%) than the control group (16.67%). Arterial wall was also thicker periodontitis group (2.22±0.35µm) (p<0.05) than the control group (1.28±0.20µm). Conclusion: Periodontitis can independently affect the coronary atherosclerotic lesion formation. ABSTRAKAnalisis histomorfometrik pembentukan lesi aterosklerosis koroner pada model tikus (Rattus novergicus) periodontitis. Penyakit kardiovaskuler perupakan penyakit paling mematikan di dunia dan penyebab utamanya adalah aterosklerosis. Paradigma baru menjelaskan bahwa inflamasi kronis seperti periodontitis dipertimbangkan sebagai faktor risiko terjadinya aterosklerosis. Periodontitis menyebabkan bakteremia yang berpengaruh terhadap inflamasi vaskuler. Keadaan ini mempengaruhi sel endotel dan oksidasi lipid sehingga meningkatkan resiko aterosklerosis. Tujuan: Penelitian ini bertujuan untuk membuktikan pengaruh periodontitis terhadap pembentukan lesi aterosklerosis koroner. Metode: Penelitian ini merupakan eksperimen menggunakan the post test only control group design. 12 sampel tikus dibagi atas kelompok kontrol (K) tanpa perlakuan dan kelompok periodontitis (P) dibuat dengan pemasangan wire ligature dan injeksi Porphyromonas gingivalis pada M1 rahang bawah kiri selama 28 hari. Pada hari ke-29 tikus didekaputasi, arteri koroner diambil dan dibuat preparat histologi. Analisis histomorfomerik dilakukan pada morfologi dungkul (deskriptif) dan ketebalan dinding arteri (statistik dengan uji T test). Hasil: Hasil penelitian menunjukkan bahwa terbentuknya dungkul arteri lebih banyak pada kelompok Periodontitis (83,33%) daripada kelompok Kontrol (16,67%). Dinding arteri kelompok periodontitis juga lebih tebal (2,22±0,35µm) secara signifikan dibandingkan kelompok kontrol (1,28±0,20µm) (p<0,05). Simpulan: Periodontitis secara independen dapat mempengaruhi gambaran histomorfometrik pembentukan lesi aterosklerosis koroner.
Increasing amount of vascular reactive oxygen species (ROS) play a key role in the pathogenesis of almost all stages of cardiovascular diseases (CVD), such as atherosclerosis, hypertension, myocardial infartion, etc. This paper aimed to present a brief review of the important vascular sources of ROS. Vascular ROS is mainly produced by enzymatic sources in the vascular cells, i.e. phagocytic inflammatory cells (neutrophils, monocytes/macrophages), and nonphagocytic cells (endothelium, smooth muscle cell and fibroblast). Enzymatic sources of vascular ROS are NADPH oxidase, xanthine oxidase, eNOS, lipoxygenase, cyclooxygenase, and mitochondrial electron transport. In conclusion, over production of ROS induce oxidative burst and will be detrimental for cardiovascular health. A better understanding of ROS would be worwhile for developing method for preventing CVD based on ROS inhibition.
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