No abstract

Aim:This study evaluated the effect of 10% ascorbic acid on the bond strength between fiber post and composite resin core after applying 24% hydrogen peroxide.Materials and Methods:Twenty-four hydrogen peroxide-treated fiber posts were divided into 4 groups (n = 6). Group 1 was the control group with no treatment. In groups 2-4, post surfaces were treated with 10% v ascorbic acid solution for 10, 30 and 60 minutes, respectively. Cores were built up using flowable composite resin. Two sticks were prepared from each specimen. Microtensile bond strength test was performed for each stick. Failure modes of sticks were evaluated under a stereomicroscope (×20). Surface morphologies of two fractured sticks from each group were assessed by SEM.Statistical analysis:Data were analyzed using one-way ANOVA and Tukey HSD tests (α = 0.05).Results:The highest microtensile bond strength was observed in Group 4 (20.55 ± 2.09) and the lowest in Group 1 (10.10 ± 0.55). There were significant differences in microtensile bond strength between all the groups (P < 0.05).Conclusion:It is concluded that ascorbic acid application increased the microtensile bond strength between the hydrogen peroxide treated fiber post and composite resin core. The increase is dependent on the duration of exposure to the antioxidant.

Background Ursodeoxycholic acid (UDCA) is one of the first‐line therapeutic medications used in treatment of cholestatic liver disease. Considering that periodontitis is epidemiologically linked to liver diseases, the question arises weather UDCA holds anti‐inflammatory properties on periodontal health. Herein, we provide information that support anti‐inflammatory effects of UDCA on three different periodontium‐related cell types. Methods Gingival fibroblasts and the oral human squamous carcinoma cell line HSC‐2 were exposed to interleukin (IL)1β and tumor necrosis factor (TNF)α with and without UDCA. Murine RAW 264.7 macrophages were incubated with sterile‐filtered human saliva also in the presence of UDCA. The expression of inflammatory cytokines was measured by reverse transcription‐polymerase chain reaction. Immunoassay was applied to detect the production of IL6. Immunostaining was performed for the p65 subunit to further support the anti‐inflammatory role of UDCA. Results We report here that UDCA significantly reduced the IL1β and TNFα‐induced expression of IL1, IL6, and IL8 in gingival fibroblasts and the HSC‐2 cell line. In RAW 264.7 macrophages, UDCA attenuated the expression of IL1α, IL1β, and IL6 that was increased by saliva. Immunoassay confirmed the capacity of UDCA to reduce inflammation‐induced production of IL6 in gingival fibroblasts, HSC‐2 and RAW 264.7 cells. Immunostaining revealed the blocking of nuclear translocation of p65 in gingival fibroblasts. Conclusions Taken together, UDCA can attenuate the provoked expression of inflammatory cytokines in oral fibroblasts, oral human squamous carcinoma cells and macrophages in vitro. These data support the hypothesis that patients with cholestatic liver disease might benefit from UDCA with respect to periodontal health.