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Martins-Porto R. Role of peroxisome proliferator activated nuclear receptor (PPAR) in induced periodontitis in rats. 2012. [Ph. D. thesis (Pharmacology)] – Instituto de Ciências Biomédicas, Universidade de São Paulo, São Paulo; 2012. Periodontitis is associated with bacteria presence (and their products) and tissue destruction caused by the host defense cells. The cytokines and arachidonic acid metabolites production play an important role in bone loss by increasing the osteoclast number. Drugs such as the antidiabetic rosiglitazone has been shown to work as an inhibitor for both the production of several inflammatory mediators (such as NO, TNF-α and IL-1β) and for osteogenesis, which occurs through PPAR-γ nuclear receptor activation. This study aimed to investigate the PPAR-γ receptor involvement on bone loss secondary to periodontitis induction, by evaluating the 21 days effects of treatment on animals with Rosiglitazone meleate (Avandia) administered by garage (vehicle CMC) and with the pure salt of rosiglitazone maleate administered intraperitoneally (vehicle DMSO). In addition, we investigated possible alterations in PPARs (α, β and γ) receptors, nitric oxide synthases isoforms (e, n and iNOS) and Osterix, RUNX2, TRAF2, TRAF6, RANKL gene expression in alveolar bone on the same animals. Twenty-one days chronic treatment with pure salt of rosiglitazone maleate (i.p) and e Avandia (v.o) increased the JEC/COA distance when compared to their respective vehicles groups. The pure salt of rosiglitazobe maleate treatment increased RANKL, nNOS, iNOS and PPAR-γ gene expression and decreased Osterix gene expression. Avandia treatment increased iNOS e PPAR-β gene expression and decreased the TRAF2 gene expression. One hour after rosiglitazone administration, we observed a higher plasma concentration when it was orally administered than when it was intraperitoneally administered. No significant differences were observed in other study periods. Three pretreatment days with DMSO were able to cause a calcium independent NOS decreased activity after 16 hours of septsemia induction. In conclusion, we suggest that rosiglitazone treatment, regardless of the administration route, exacerbated secondary bone loss to periodontitis assessed seven days after disease induction. This increase is probably due to iNOS, RANKL and TRAF6 increased gene expression (related osteoblast activity), and Osterix decreased gene expression (osteoblast activity). Discrepancies with published results by others authors may be due DMSO interference in the treatment composition, which was demonstrated in this study by different signaling pathways observed for each administration route used.

Papel dos receptores nucleares ativados por proliferadores de peroxissomos (PPAR) na periodontite induzida em ratos.