| Grant number: | 15/07107-0 |
| Support Opportunities: | Scholarships abroad - Research Internship - Doctorate |
| Start date: | December 01, 2015 |
| End date: | November 30, 2016 |
| Field of knowledge: | Health Sciences - Dentistry - Endodontics |
| Principal Investigator: | Luciano Tavares Angelo Cintra |
| Grantee: | Mariane Maffei Azuma |
| Supervisor: | Toshihisa Kawai |
| Host Institution: | Faculdade de Odontologia (FOA). Universidade Estadual Paulista (UNESP). Campus de Araçatuba. Araçatuba , SP, Brazil |
| Institution abroad: | Forsyth Institute, United States |
| Associated to the scholarship: | 13/26390-0 - Local and systemic influence of dietary supplementation with omega - 3 in rats with endodontic infection, BP.DR |
Abstract Periapical periodontitis is an infectious disease characterized by inammatory bone destruction that is mediated by bacteria-reactive lymphocytes. A growing body of evidence supports that osteoclastogenesis factor, receptor activator of nuclear factor kappa B (NF-kB) ligand (RANKL), produced by activated lymphocytes is responsible for the induction of bone resorption in periapical periodontitis. The sufficiently and efficiently performed root canal treatment can get rid of bacteria from infected root which, in turn, reduce the local production of RANKL by bacteria-reactive lymphocytes. However, even after the appropriate procedures of root canal treatment, new bone formation in the periapical lesion is, in general, slow and insufficient. On the other hand, recent studies discovered that Semaphorin 4D (Sema4D) produced by osteoclasts can counteract the new bone formation by suppressing the IGF-1-induced bone anabolic signals in osteoblasts. Importantly, IGF-1 is not only produced by liver, but also released from bone matrix after the bone resorption caused by osteoclasts. We hypothesized that Sema4D expression is upregulated in the bone resorption lesion of periapical periodontitis which may interrupt the new bone formation. The proposed study will investigate the expression patterns of Sema4D as well as its possible downregulatory role in new bone formation in the context of periapical bone destruction using a mouse model of periradicular periodontitis. (AU) | |
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