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.

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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.

Orthodontic tooth movement in a rodent model is reduced by lithium chloride (LiCl), a mood-stabilizing agent with antithyroid effects. Considering the established inhibitory effect of N(omega)-nitro-L-arginine methyl ester (L-NAME) on orthodontic tooth movement and the possible role of nitric oxide synthase in LiCl mechanism of action, the question arises if these two mechanisms are synergistic. To answer this question, 70 male Sprague Dawley rats were randomly divided into seven groups: untreated group without any interventions (i), and the orthodontic tooth movement groups receiving daily saline injection (ii), 300 (iii), and 600 mg/kg (iv) of LiCl per os, 10 mg/kg of L-NAME (v) and the combinations of 300 (vi) and 600 mg/kg LiCl (vii) with L-NAME. The first molar was moved towards the incisor with 60 g of mesial tipping force applied by an activated fixed coil spring for two weeks. The resulted distance between the first and the second molar was measured using a feeler gauge. The serum parameters were also determined. We report here that both concentrations of LiCl significantly decreased tooth movement. Even though L-NAME was capable of reducing orthodontic tooth movement, no synergistic effects with LiCl were observed. Moreover, L-NAME had no impact on the robust and significant increase of thyroid-stimulating hormone (TSH) and decrease of triiodothyronine (T3) and thyroxine (T4) in the LiCl treated rats. These findings suggest LiCl significantly decreases the orthodontic tooth movement in rats; however, this ability seems not to be principally mediated through nitric oxide synthase.

PURPOSEThe aim of the present study was to assess the effect of ascorbic acid, ethanol and acetone on microtensile bond strength between fiber posts pre-treated with hydrogen peroxide and composite resin cores.MATERIALS AND METHODSTwenty four fiber posts were pre-treated with 24% hydrogen peroxide and divided into 4 groups as follows: G1: no treatment, as control group; G2: treatment with 10% ascorbic acid solution for 5 minutes; G3: treatment with 70% ethanol solution for 5 minutes; and G4: treatment with 70% acetone solution for 5 minutes. Each fiber post was surrounded by a cylinder-shaped polyglass matrix which was subsequently filled with composite resin. Two sections from each sample were selected for microtensile test at a crosshead with speed of 0.5 mm/min. Statistical analyses were performed using one-way ANOVA and a post hoc Tukey HSD test. Fractured surfaces were observed under a stereomicroscope at ×20 magnification. The fractured surfaces of the specimens were observed and evaluated under a SEM.RESULTSMeans of microtensile bond strength values (MPa) and standard deviations in the groups were as follows: G1: 9.70±0.81; G2: 12.62±1.80; G3: 16.60±1.93; and G4: 21.24±1.95. G4 and G1 had the highest and the lowest bond strength values, respectively. A greater bond strength value was seen in G3 compared to G2. There were significant differences between all the groups (P<.001). All the failures were of the adhesive mode.CONCLUSIONApplication of antioxidant agents may increase microtensile bond strength between fiber posts treated with hydrogen peroxide and composite cores. Acetone increased bond strength more than ascorbic acid and ethanol.

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Objectives Chronic liver disease increases the risk for periodontal disease and osteoporotic fractures, but its impacts on bone regeneration remain unknown. Herein, we studied the impact of liver cirrhosis on peri‐implant bone formation. Material and Methods A total of 20 male Wistar rats were randomly divided into two groups: one with the common bile duct ligated (BDL) and the respective sham‐treated control group (SHAM). After four weeks of disease induction, titanium mini‐screws were inserted into the tibia. Successful induction of liver cirrhosis was confirmed by the presence of clinical symptoms. Another four weeks later, peri‐implant bone volume per tissue volume (BV/TV) and bone‐to‐implant contact (BIC) were determined by histomorphometric analysis. Results Peri‐implant bone formation was not significantly different between the SHAM and BDL groups. In the cortical compartment, the median percentage of peri‐implant new bone was 10.1% (95% CI of mean 4.0–35.7) and 22.5% (13.8–30.6) in the SHAM and BDL groups, respectively (p = .26). Consistently, the new bone in direct contact with the implant was 18.1% (0.4–37.8) and 23.3% (9.2–32.8) in SHAM and BDL groups, respectively (p = .38). When measuring the medullary compartment, the new bone area was 7.1% (4.8–10.4) and 10.4% (7.2–13.5) in the SHAM and BDL groups, respectively (p = .17). Medullary new bone in direct contact with the implant was 10.0% (1.2–50.4) and 20.6% (16.8–35.3) in SHAM and BDL groups, respectively, and thus comparable between the two groups (p = .46). Conclusions Bile duct ligation has no significant impact on the early stages of peri‐implant bone formation.

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