Bone healing around titanium implants in a preclinical model of bile duct ligation-induced liver injury.

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.

Taurocholic acid lowers the inflammatory response of gingival fibroblasts, epithelial cells, and macrophages.

Taurocholic acid (TCA), a conjugation of cholic acid with taurine, is one of the main bile acids that is elevated in liver disease. Considering the epidemiologic linkage of periodontal disease to liver disease, the question arises about the possible effect of elevated TCA levels on periodontal cells. To answer this question, gingival fibroblasts and human oral squamous cell carcinoma cell line (HSC-2) were pretreated with interleukine1ß (IL1ß) and tumor necrosis factorα (TNFα) in the presence and absence of TCA. Also, mouse macrophages (RAW 264.7) were incubated with sterile-filtered human saliva with and without TCA. Inflammatory cytokines were measured by real time polynucleotide chain reaction (RT-PCR) and an immunoassay. The nuclear translocation of the p65 subunit was visualized by immunostaining. In pretreated gingival fibroblasts and HSC-2 cells, TCA considerably reduced the expression of IL1ß, IL6, and IL8. In support of these observations, TCA lowered the saliva-induced expression of IL1α, IL1ß and IL6 in RAW 264.7 cells. An immunoassay confirmed the capacity of TCA to diminish inflammation-induced expression of IL6 in gingival fibroblasts, HSC-2 and RAW 264.7 cells. Consistently, TCA blocked the nuclear translocation of p65 in fibroblasts. These findings suggest that TCA has anti-inflammatory activity in gingival fibroblasts, human oral squamous cell carcinoma cells and macrophages in vitro.

Ursodeoxycholic acid attenuates the expression of proinflammatory cytokines in periodontal cells.

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)1ß 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 IL1ß 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, IL1ß, 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.

Effect of ascorbic acid on bond strength between the hydrogen peroxide-treated fiber posts and composite resin cores.

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.

Effect of ascorbic acid, ethanol and acetone on adhesion between the treated fiber posts and composite resin cores.

PURPOSE: The 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 METHODS: Twenty 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. RESULTS: MEANS 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. CONCLUSION: Application 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.

Effect of ascorbic acid, ethanol and acetone on adhesion between the treated fiber posts and composite resin cores

PURPOSE: The 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 METHODS: Twenty 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 x20 magnification. The fractured surfaces of the specimens were observed and evaluated under a SEM. RESULTS: Means 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. CONCLUSION: Application 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.