Periodontitis-induced lipid peroxidation in rat descending aorta is involved in the initiation of atherosclerosis.
OBJECTIVE
Periodontitis is a risk factor for the development of atherosclerosis. Recent studies indicate that oxidative mechanisms, including lipid peroxidation, are involved not only in periodontitis but also in atherosclerosis. Lipid peroxidation may play an important role in the pathogenesis of atherosclerosis, particularly during its earliest stages. The purpose of this study was to investigate the relationship between lipid peroxidation induced by periodontitis and the initiation of atherosclerosis.


METHODS
Sixteen rats were randomly divided into two groups of eight rats each. Periodontitis was ligature-induced for 4 wk in the experimental group, whereas the control group was left untreated. After the experimental period, the mandibular first molar regions were resected and then subjected to histological analysis and measurement of hexanoyl-lysine expression as an indicator of lipid peroxidation. Descending aorta was used for measuring the levels of hexanoyl-lysine, reactive oxygen species and lipid deposits, and for real-time polymerase chain reaction microarray analysis. The level of hexanoyl-lysine was also measured in serum.


RESULTS
In the experimental group, the levels of hexanoyl-lysine in periodontal tissue and serum increased. Only aorta samples in the experimental group showed lipid accumulation, with increased expression of hexanoyl-lysine, reactive oxygen species and oxidative stress-related genes (including nitric oxide synthases 2 and 3), whereas the superoxide dismutase 1 gene level was down-regulated.


CONCLUSIONS
In a ligature-induced periodontitis rat model, increased lipid peroxidation was found in serum and aorta as well as in periodontal tissue. Atherosclerosis-related gene expression and histological changes were also stimulated. Periodontitis-induced lipid peroxidation in the aorta may be involved in the early stage of atherosclerosis.
Ekuni
D
D
Department of Preventive Dentistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan.
Tomofuji
T
T
Sanbe
T
T
Irie
K
K
Azuma
T
T
Maruyama
T
T
Tamaki
N
N
Murakami
J
J
Kokeguchi
S
S
Yamamoto
T
T
D000818:Animals; D001013:Aorta, Thoracic / Q000378:metabolism* / Q000473:pathology; D001018:Aortic Diseases / Q000209:etiology* / Q000378:metabolism / Q000473:pathology; D050197:Atherosclerosis / Q000209:etiology* / Q000378:metabolism / Q000473:pathology; D004195:Disease Models, Animal; D015536:Down-Regulation; D005347:Fibroblasts / Q000378:metabolism / Q000473:pathology; D006861:Hydrogen Peroxide / Q000032:analysis; D015227:Lipid Peroxidation / Q000502:physiology*; D008055:Lipids / Q000032:analysis; D008239:Lysine / Q000032:analysis / Q000097:blood; D008297:Male; D046228:Microarray Analysis; D008963:Molar / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II / Q000032:analysis; D052250:Nitric Oxide Synthase Type III / Q000032:analysis; D018384:Oxidative Stress / Q000502:physiology; D010513:Periodontal Ligament / Q000378:metabolism / Q000473:pathology; D010518:Periodontitis / Q000378:metabolism* / Q000473:pathology; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D017382:Reactive Oxygen Species / Q000032:analysis; D013482:Superoxide Dismutase / Q000032:analysis; D000072105:Superoxide Dismutase-1
D008055:Lipids; C120589:N(epsilon)-hexanoyllysine; D017382:Reactive Oxygen Species; D006861:Hydrogen Peroxide; D052247:Nitric Oxide Synthase Type II; D052250:Nitric Oxide Synthase Type III; C496316:Nos3 protein, rat; C000606292:Sod1 protein, rat; D013482:Superoxide Dismutase; D000072105:Superoxide Dismutase-1; D008239:Lysine