[Effect of hydroxyapatite based agents on the bonding properties of universal adhesives].

Objective: To study the effect of hydroxyapatite (HA) based agents on the bonding properties of universal adhesive with different application modes, and to provide evidence for the use of adhesives after desensitization treatment. Methods: Sixty impacted third molars were extracted and selected (acquired from Department of Oral and Maxillofacial Surgery, College of Stomatology, Xi'an Jiaotong University). Four third molars were used to prepare 1 mm thick dentin disks and treated with 1% citric acid to simulate sensitive tooth models. The dentin surfaces were observed by scanning electron microscope (SEM) after treating with no desensitization (control group), desensitized by HA based toothpaste Biorepair and Dontodent Sensitive respectively (desensitizing toothpaste A group and B group), or HA paste treatment (desensitizing paste group ) (n=2 per group). The remaining teeth were selected to expose the mid-coronal dentin and establish dentin sensitivity models. Then, the specimens were divided into 4 former groups and received corresponding treatment. Each group was randomly divided into 2 subgroups, and intermediately strong universal adhesive (G-Premio Bond) was applied on the desensitized dentin by either etch-and-rinse mode or self-etch mode. Resin-dentin slice specimens (n=4 per subgroup), microtensile specimens (n=20 per subgroup) and slice specimens (n=6 per subgroup) were prepared. The microstructure and nanoleakage of the adhesive interfaces were observed by scanning electron microscopy (SEM). The microtensile strength (bond strength) and fracture mode were tested and recorded. The water permeability of the adhesive interface was observed by laser scanning confocal microscopy (LSCM). Results: SEM showed that desensitizing toothpaste and desensitizing paste could partially or entirely occlude most of the dentin tubules. For the etch-and-rinse mode, the bond strength of specimens treated with toothpaste A [(40.98±4.60) MPa], toothpaste B [(40.89±4.64) MPa] and HA paste [(41.48±3.65) MPa] was significantly higher than that of the control group [(38.58±4.28) MPa] (F=3.89,P<0.05). There was no statistically significant difference in bond strength among the 4 subgroups for self-etch modes (F=0.48,P>0.05). After desensitization, the bond strength of the control group and desensitizing groups in the self-etch mode was significantly higher than that in the etch-and-rinse mode (P<0.05). The overall fracture modes were mixed failure and interfacial failure in the control group and desensitizing groups. SEM showed speckled silver-stained particles deposited along the bottom of the hybrid layer on the bond interface of etch-and-rinse mode, and there were few silver-stained particles deposited on the bond interface of self-etch mode. LSCM showed continuous linear penetration in the hybrid layer of etch-and-rinse mode subgroups and discontinuous linear penetration in the hybrid layer of self-etch mode subgroups. Conclusions: HA based desensitizers have no adverse effect on the bond strength of intermediately strong universal adhesive and show good bonding performance accompanied with the self-etch mode.

[Effect of a nano hydroxyapatite desensitizing paste application on dentin bond strength of three self-etch adhesive systems].

Objective: To evaluate a nano-hydroxyapatite (nano-HA) desensitizing paste application on the bond strength of three self-etch adhesives. Methods: Three dentin specimens of about 1 mm thick were cut from two teeth. Scanning electron microscope (SEM) was used to evaluate the dentin surfaces without treatment, after citric acid treatment and after nano-HA treatment. Thirty-six intact third molars extracted for surgical reasons were cut to remove the occlusal enamel with isomet, and then were etched with 1% citric acid for 20 s to simulate the sensitive dentin and divided into two groups randomly using a table of random numbers (n=18): the control group (no treatment) and the HA treated group (with nano-HA paste treatment). Each group was divided into three subgroups randomly using a table of random numbers (n=6). Subgroup A, B and C was bonded with G-Bond, Clearfil S(3) Bond and FL-Bond Ⅱ according to the manufacture's instruction separately. At 24 h after bonding procedure, and after water storage for 6 months, microtensile bond strength of the specimens was tested and the failure mode was analyzed. Results: SEM obeservation showed that citric acid could open the dentin tubules to set up the sensitive dentin model, and the nano-HA could occlude the dentin tubules effectively. For subgroup A, bonding strength of specimens treated with nano-HA ([41.14±8.91] MPa) was significantly high than that of the control group ([34.27±6.16] MPa) at 24 h after bonding procedure (P<0.05). However, after 6 month water ageing, the bonding strength of the control group and the HA treated group showed no significant difference (P>0.05). For subgroup B, specimens with nano-HA application showed lower bonding strength ([30.87±6.41] MPa) than that of the control group ([36.73±5.82] MPa) at 24 h after bonding procedure (P<0.05), and after 6 month water ageing, the bond strength of nano-HA application ([25.73±6.99] MPa) was also lower than that of the control group ([32.33±5.08] MPa) (P<0.05). For subgroup C, the bond strength of the control group and the HA treated group have no significant difference either before or after 6 month water ageing (P>0.05). Failure mode analysis showed that more than half of the samples in all groups were adhesive failure. Conclusions: Nano-HA treatment decreased the bond strength of subgroup B, while had no adverse effect on subgroup A and subgroup C.

[Effect of epigallocatechin-3-gallate on the proliferation and osteogenesis of human periodontal ligament cells].

Objective: To evaluate the effect of epigallocatechin-3-gallate (EGCG) treatment on the proliferation and osteogenic differentiation of human periodontal ligament cell (hPDLC) and to explore the potential role of EGCG in promoting periodontal hard tissue regeneration. Methods: The hPDLC was isolated from periodontal ligament tissue obtained from freshly extracted human teeth. The effect of treatments with various concentrations of EGCG (0 µmol/L, 2 µmol/L, 4 µmol/L, 6 µmol/L, 8 µmol/L and 10 µmol/L) on cell proliferations were determined by cell counting kits (CCK) after 24-, 48- and 72-hour-incubations, respectively. Osteogenic differentiation abilities of hPDLCs were assessed by using alkaline phosphatase (ALP) activity tests after 7- and 14-day-incubations, respectively. The mineralized nodules were quantitatively examined and analyzed by using alizarin red staining after 21-day-incubation. The real-time PCR (RT-PCR) assays were conducted fordetecting the expressions of Runt related transcription factor-2 (Runx2), ALP and collagen type Ⅰ (COL Ⅰ) after 7-day-incubation. Results: Treatment with 4 µmol/L EGCG increased hDPLC proliferation at 24 h, while 8 µmol/L or 10 µmol/L EGCG treatment groups showed inhibiting effects at 24 h and 72 h, respectively. Findings of alizarin redstaining showed orange to red colored extracellular mineralized nodules in all groups. The the A values of 2, 4, 6, 8, 10 µmol/L EGCG groups were 0.119±0.001, 0.167±0.003, 0.173±0.003, 0.110±0.001 and 0.083±0.003, respectively. A values of 2-8 µmol/L EGCG groups were significantly higher than that of the control group, however there was no significant difference of the A values between10 µmol/L EGCG group and the control group (0.077±0.001). Treatments with 2-10 µmol/L EGCG could significantly increase the mRNA expressions of COL Ⅰ and ALP with the highest values in 4-6 µmol/L EGCG treatment groups. Although treatments with 4 and 6 µmol/L EGCG both could increase the mRNA expressions of Runx2, the result in 4 µmol/L group was much better than that of 6 µmol/L group. Conclusions: Treatment of 4 µmol/L EGCG could promote hPDLC proliferation at early stageand treatments with 4-6 µmol/L EGCG could significantly promote the osteogenesis of hPDLCs which might play a promising role in periodontal hard tissue regeneration.