TY - JOUR
T1 - Occlusal disharmony accelerates the initiation of atherosclerosis in apoE knockout rats
AU - Ekuni, Daisuke
AU - Yoneda, Toshiki
AU - Endo, Yasumasa
AU - Kasuyama, Kenta
AU - Irie, Koichiro
AU - Mizutani, Shinsuke
AU - Azuma, Tetsuji
AU - Tomofuji, Takaaki
AU - Morita, Manabu
N1 - Funding Information:
This work was supported by the Uehara Memorial Foundation, Tokyo, Japan. The authors report no conflicts of interest with regard to this study.
Publisher Copyright:
© 2014 Ekuni et al.; licensee BioMed Central Ltd.
PY - 2014/9/5
Y1 - 2014/9/5
N2 - Background: Psychosocial stress is one of the risk factors for atherosclerosis. As occlusal disharmony induces psychological stress, we hypothesized that psychological stress by occlusal disharmony accelerates atherosclerosis. The aim of this study was to investigate the effects of occlusal disharmony on the initiation of atherosclerosis in apolipoprotein E (apoE) knockout rats. Methods: Fourteen male apoE-knockout rats (age; 8 weeks) (Sprague-Dawley strain background) were divided into two groups of seven rats: the occlusal disharmony group and the no treatment (control) group. In the occlusal disharmony group, the maxillary molar cusps were cut off for the 8-week experimental period. Results: In the occlusal disharmony group, the percentages of the area of total aortic lumen occupied by plaques and lipid were significantly higher than those in the control group (p < 0.05, t-test). The occlusal disharmony group also showed significantly higher serum levels of very low-density lipoprotein-cholesterol (VLDL) and low-density lipoprotein-cholesterol (LDL), plasma levels of corticosterone (1.9, 1.3 and 1.3 times, respectively), higher aortic protein expression levels of vascular cell adhesion molecule-1 (VCAM1) and intercellular adhesion molecule-1 (ICAM1) (1.5 and 1.4 times, respectively), and higher aortic gene expression of levels of VCAM1 and Toll-like receptor 4 ( TLR4) (1.9 and 4.3 times, respectively), as compared to the control group (p < 0.05). However, there were no significant differences in serum levels of oxidized LDL, reactive oxygen metabolites and C-reactive protein between the two groups. Conclusion: In apoE knockout rats, occlusal disharmony may induce VCAM1, ICAM1 and TLR4 expression and accelerate the initiation of atherosclerosis.
AB - Background: Psychosocial stress is one of the risk factors for atherosclerosis. As occlusal disharmony induces psychological stress, we hypothesized that psychological stress by occlusal disharmony accelerates atherosclerosis. The aim of this study was to investigate the effects of occlusal disharmony on the initiation of atherosclerosis in apolipoprotein E (apoE) knockout rats. Methods: Fourteen male apoE-knockout rats (age; 8 weeks) (Sprague-Dawley strain background) were divided into two groups of seven rats: the occlusal disharmony group and the no treatment (control) group. In the occlusal disharmony group, the maxillary molar cusps were cut off for the 8-week experimental period. Results: In the occlusal disharmony group, the percentages of the area of total aortic lumen occupied by plaques and lipid were significantly higher than those in the control group (p < 0.05, t-test). The occlusal disharmony group also showed significantly higher serum levels of very low-density lipoprotein-cholesterol (VLDL) and low-density lipoprotein-cholesterol (LDL), plasma levels of corticosterone (1.9, 1.3 and 1.3 times, respectively), higher aortic protein expression levels of vascular cell adhesion molecule-1 (VCAM1) and intercellular adhesion molecule-1 (ICAM1) (1.5 and 1.4 times, respectively), and higher aortic gene expression of levels of VCAM1 and Toll-like receptor 4 ( TLR4) (1.9 and 4.3 times, respectively), as compared to the control group (p < 0.05). However, there were no significant differences in serum levels of oxidized LDL, reactive oxygen metabolites and C-reactive protein between the two groups. Conclusion: In apoE knockout rats, occlusal disharmony may induce VCAM1, ICAM1 and TLR4 expression and accelerate the initiation of atherosclerosis.
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U2 - 10.1186/1476-511X-13-144
DO - 10.1186/1476-511X-13-144
M3 - Article
C2 - 25189624
AN - SCOPUS:84908217116
SN - 1476-511X
VL - 13
JO - Lipids in Health and Disease
JF - Lipids in Health and Disease
IS - 1
M1 - 144
ER -
