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Int J Oral Biol. 2012 Jun;37(2):63-68. Korean. Original Article.
Bak EJ , Kim JH , Lee DE , Park BH , Ryu JH , Cha JH , Jeon R , Yoo YJ .
Oral Cancer Research Institute, Yonsei University College of Dentistry, Seoul, Korea.
Research Center for Orofacial Hard Tissue Regeneration, College of Dentistry, Yonsei University, Seoul, Korea. yu618@yuhs.ac
Department of Oral Biology, Oral Science Research Center, Yonsei University College of Dentistry, Seoul, Korea.
Department of Applied Life Science, The Graduate School, Yonsei University, Seoul, Korea.
Department of Biochemistry, Chonbuk national University Medical School, Jeonju, Korea.
Research Center for Cell Fate Control, College of Pharmacy, Sookmyung Women's University, Seoul, Korea.
Abstract

It has been documented that SPA0355 exerts anti-inflammatory effects via the inhibition of nuclear factor-kappaB activation. In present study, we investigated the inhibitory effects of SPA0355 on periodontitis in an animal model. Periodontitis was induced by ligation of the cervix of the 1st molar in the left mandible in rats. After ligature, the rats were randomly divided into four groups and topically applied with SPA0355 (0.5, 1, and 2%) or the vehicle alone once daily for 10 days. Body weight and food intake were measured daily throughout the experimental period. At day 10 post-ligature, the infiltration of inflammatory cells and distance of the cementoenamel junction (CEJ) to the alveolar bone crest (ABC) in the distal area of ligatured tooth were estimated histopathologically. No changes in body weight or food intake were found between the control and SPA0355 groups. The degree of inflammation was decreased in all three SPA0355 application groups. A decrease CEJ-ABC distance was observed in the 0.5% and 1% SPA0355 groups. These results indicate that SPA0355 inhibits the infiltration of inflammatory cells and alveolar bone resorption and suggests its potential as a therapeutic agent for periodontitis.

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