|Support type:||Scholarships in Brazil - Post-Doctorate|
|Effective date (Start):||October 01, 2013|
|Effective date (End):||September 30, 2014|
|Field of knowledge:||Health Sciences - Dentistry - Periodontology|
|Principal Investigator:||Luis Carlos Spolidorio|
|Grantee:||João Paulo Steffens|
|Home Institution:||Faculdade de Odontologia (FOAr). Universidade Estadual Paulista (UNESP). Campus de Araraquara. Araraquara , SP, Brazil|
The etiopathogenesis of the immune-inflammatory responses associated with periodontal disease is a strictly regulated and complex process that involves many molecules related with different cell signaling pathways. In this context, the interaction of hormones and their receptors, including sex hormones, plays an important role. It is plausible that androgenic hormones role on immune-inflammatory responses is based on a complex interaction network that culminates in host response modulation. Particularly, our group demonstrated that sub- and supraphysiologic androgen levels exacerbate the immune-inflammatory response and periodontal bone loss using a ligature-induced periodontitis model in male rats. Besides, we reported that physiologic levels of testosterone inhibit osteoclastogenesis both directly and indirectly, reducing osteoblast-derived RANKL expression in vitro. Despite the biological plausibility in the participation of androgenic hormones playing an active role on the etiopathogenesis of periodontal diseases, little is known about the importance of androgens on the different events that take place during the progression and reparative phases of periodontal disease in females. This project aims to extend our studies inhibiting androgen and estrogen receptors or administering testosterone with or without aromatase inhibitor in female rats. As research tools, we will evaluate the systemic bone metabolism biochemical profile, hormone modulation, and will perform cell and molecular biology experiments to evaluate the immune-inflammatory and bone metabolism responses in periodontal health, disease and repair.