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Role of tumor necrosis factor-alfa in pulpal and periapical inflammation and repair

Grant number: 19/00204-1
Support type:Regular Research Grants
Duration: June 01, 2019 - May 31, 2021
Field of knowledge:Health Sciences - Dentistry
Principal Investigator:Francisco Wanderley Garcia de Paula e Silva
Grantee:Francisco Wanderley Garcia de Paula e Silva
Home Institution: Faculdade de Odontologia de Ribeirão Preto (FORP). Universidade de São Paulo (USP). Ribeirão Preto , SP, Brazil

Abstract

Tumor necrosis factor-z (TNF-z) role in in vitro induction of dental pulp cell proliferation, migration and differentiation of dental pulp cells is already known and indicates that this mediator might be and important regulator of the recruitment of cells to injured sites for tissue regeneration or repair. Nevertheless, all these phenomena were demonstrated in vitro in cell culture models, opening avenues for in vivo investigation. Therefore, the general goal of this research is to investigate the role of TNF-z in dental pulp inflammation and repair and in the development of apical periodontitis, using genetically deficient mice to TNF-z receptor-1 (TNFRSF1) in comparison to wild type animals (C57Bl6). A pulp capping model will be used to evaluate the dental pulp response after tissue exposure and protection. To evaluate the periapical bone response, a model will be used in which the pulp tissue will be exposed to the buccal environment for microbial contamination. The specific objectives will be to investigate: (i) the degree of tissue inflammation by quantifying inflammatory cells and evaluating gene and protein expression, (ii) microbial contamination in pulp and periapical tissues, (iii) reabsorption of mineralized tissues by computerized microtomography and microscopic analysis, and (iv) osteoclastogenesis on bone tissue and dental root surfaces. In addition, TNF-z estimulated dental pulp cells will be used to dissect the possible mechanisms involved in the regulation of proteins important for the mineralization process under pro-inflammatory stimuli. (AU)