Impact of natural curcumin on the progression of experimental periodontitis in diabetic rats.

OBJECTIVE: To evaluate the role of natural curcumin (CURC) on experimental periodontitis (EP) in animals with diabetes mellitus (DM). MATERIAL AND METHODS: One hundred rats were assigned to DM + placebo (PLA); DM + CURC; DM + insulin (INS); DM + CURC + INS; and Non-DM. Diabetes was induced by streptozotocin. After 3 days, they were initiated CURC and PLAC solutions and insulin administrations, daily for 30 days. This included a period of 19 days prior to EP induction (ligature at the first mandibular and the second maxillary molar) and then additional 11 days. Specimens from the mandible were processed for morphometric examination of bone level. Gingival tissues from mandibular molars were collected for quantification of IL-1ß, IL-4, IL-6, IL-17, IFN-γ, and TNF-α using a Luminex/MAGpix assay. Gingivae from maxillary molars were subjected to RT-PCR for assessment of Runx2, RANKL, OPG, SIRT, Dkk1, and Sost levels. RESULTS: Lower linear bone loss was detected in ligated molars of DM + CURC + INS vs DM + PLAC and DM + INS groups (P < 0.05). In ligated sites from DM rats treated with CURC + INS, IL-6, IL-1ß, INF-γ, and TNF-α levels were the lowest in comparison with PLAC and/or INS and CURC as monotherapies (P < 0.05). CURC, independently of INS, increased Runx2 and SIRT when compared to DM + PLAC (P < 0.05) in ligated sites, whereas only CURC + INS reduced the RANKL/OPG ratio when compared to DM + PLAC (P < 0.05). CONCLUSION: Natural CURC, when associated with INS, reduces the DM-induced loss of supporting alveolar bone and promotes favorable modulation on osteo-immune-inflammatory mediators.

Resveratrol Inhibits Periodontitis-Related Bone Loss in Rats Subjected to Cigarette Smoke Inhalation.

BACKGROUND: Alternative therapeutic approaches have been explored to modulate host response to periodontal disease. Knowledge of new strategies to treat periodontitis is particularly relevant in patients presenting augmented risk to periodontitis, such as smokers. The aim of this study is to investigate the impact of resveratrol (RESV) on progression of experimental periodontitis (EP) in the presence of cigarette smoke inhalation (CSI). METHODS: Rats were assigned to one of three groups: 1) CSI+RESV (n = 20); 2) CSI+placebo (n = 20); and 3) non-CSI (n = 20). CSI was initiated 1 week prior to initiation of RESV or placebo administration (systemically for 30 days) and was continued until the end of the study. EP was induced around the first mandibular and second maxillary molars using ligatures. Specimens from the mandible were processed for morphometric and microcomputed tomography examination of bone volume/levels. Gingival tissues surrounding mandibular molars were collected for quantification of interleukin (IL)-1ß, IL-4, IL-6, IL-17, and tumor necrosis factor-α using an assay system. Additional analyses of immunoinflammatory mediator performance (T-helper Type 17 [Th17]/Th2 and Th1/Th2 cell levels) were performed according to Th cell responses in gingival tissues. Gingival tissues of maxillary molars were subjected to real-time polymerase chain reaction for assessment of osteoprotegrin, runt-related transcription factor-2, receptor activator of nuclear factor-kappa B ligand (RANKL), sclerostin, and Dickkopf Wnt signaling pathway inhibitor 1 levels. RESULTS: Higher linear alveolar bone loss (ABL) and lower interradicular bone density were detected in ligated molars in the CSI+placebo group (P <0.05). IL-4 level was the highest, and Th17/Th2 levels were the lowest in RESV-treated rats compared with placebo rats (P <0.05). RESV reduced expression of messenger RNA for RANKL in animals receiving CSI (P <0.05). CONCLUSION: RESV inhibits EP and CSI-induced supporting ABL and has a beneficial effect on osteo-immunoinflammatory markers.