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Role of TLR and NLR complex in the process of alveolar bone repair in mice

Grant number: 12/16404-0
Support type:Scholarships in Brazil - Post-Doctorate
Effective date (Start): November 01, 2012
Effective date (End): May 31, 2014
Field of knowledge:Health Sciences - Dentistry
Principal Investigator:Gustavo Pompermaier Garlet
Grantee:Carlos Eduardo Palanch Repeke
Home Institution: Faculdade de Odontologia de Bauru (FOB). Universidade de São Paulo (USP). Bauru , SP, Brazil

Abstract

The acceleration of bone formation in repair process is a major challenge in health care. Several studies are being conducted to find a faster and more efficient process of bone formation. One of these is the modulation of the immune/inflammatory response. However, the balance between the process of bone healing and inflammatory response appears to be extremely important and complex, although poorly understood. With the discovery of signaling via Toll-like receptors (TLRs) and Nod-like receptors (NLRs) opened a huge window for studying the relationship between immune system and bone tissue. Since, we have noted these receptors play an important role in the early immune/inflammatory response through the recognize of Pathogen-associated molecular patterns (PAMPs) and Damage associated molecular pattern (DAMPs) molecules. In addition, this recognition is able to induce several inflammatory mediators such as cytokines and chemokines that influence positively osteoclastogeneses and consequently on bone resorption. On the one hand, the blockage of TLRs and NLRs signaling seems something positive and efficient, it is important to remember the immune/inflammatory response is fundamental in the blood clot removal and in the future bone tissue formation in bone repair process. Therefore, questions are being formed and requiring more knowledge about immune/inflammatory response process, as well as its modulation and its components role in the bone tissue repair. In the present study we aim to elucidate the importance of the immune/inflammatory response that triggered by PAMPs and DAMPs, released during the upper incisor tooth extraction of mice. In this way, we will use genetically deficient mice for MyD88, RICK and Caspase 1, molecules fundamental for the TLRs and NLRs signaling, respectively. The results of molecular and histomorphometric analysis will certainly contribute to the improvement of knowledge of molecular and cellular mechanisms involved in immune/inflammatory response which is necessary for bone tissue repair. So, it will expand the broad spectrum of the scientific scenario, not only for future drugs development, but also in the individualization of trauma and bone diseases treatment.