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Advanced Glycation End-product Affects Calcification and Inflammation in Rat Dental Pulp Tissues
Nakajima, Yukiko Department of Periodontology and Endodontology, Institute of Health Biosciences, University of Tokushima Graduate School Tokushima University Educator and Researcher Directory KAKEN Search Researchers
Amorphous calcification frequently appears in dental pulp tissues of diabetic patients.
Diffuse calcifications and pulp stones may block access to canal orifices and alter the internal anatomy. It has been demonstrated that careful instrumentation is required to remove pulp stones for the successful endodontic therapy. Dental pulp pain often appears in diabetic patients and is referred to as diabetic odontalgia. Diabetic pulp is generally more likely to have impaired collateral circulation and reduced microbicidal polymorphonuclear leucocyte activity. These disorders increase the risk of ischemia, infection, and necrosis; therefore, pulpal infection may be considered as anachoresis.
However, its pathologic process has not been fully elucidated. Advanced glycation end-products (AGE) have been found to play a role in the progression of diabetic vascular complications and inflammation.
We examined AGE-effect on the expression of calcification and inflammation factors using rat dental pulp tissues and cell cultures. Expressions of RAGE, OPN, OCN, BSP, DSPP, S100A8, S100A9, IL-1β, IL-6 and TNF-α mRNAs increased both in diabetic dental pulp tissues and in dental pulp cultures treated with AGE. ALPase activity and calcium deposition increased by the treatment with AGE in dental pulp cells. In the presence of anti-RAGE antibody or siRNA for RAGE, AGE did not increase in OPN, OCN, S100A8 or S100A9 expressions. The AGE-induced increases in OPN, OCN, S100A8 and S100A9 were inhibited by MAPK inhibitor. These results indicated that AGE may be a stimulatory factor of pathologic calcification and inflammation in diabetic dental pulp tissues and the effect is characteristic in dental pulp cells. Additionally, AGE may be associated with the RAGEMAPK signaling pathway.
Journal of Oral Health and Biosciences
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