Effect of polydopamine and fluoride ion coating on dental enamel remineralization: an in vitro study.

BACKGROUND: Fluoride treatment is one of the most effective dental caries prevention methods. To continuously prevent dental caries, stably immobilizing the fluoride on the tooth enamel is highly desirable. This study aimed to evaluate the remineralization of tooth enamels by one-pot coating using polydopamine and fluoride ions. METHODS: To prepare the enamel specimens for polydopamine- and fluoride ion-coating, they were treated with polydopamine- and fluoride-containing gels. The enamel specimens were collected from human molars in a blind manner (n = 100) and were randomized into five treatment groups (n = 20, each): 1) untreated, 2) polydopamine-coated, 3) fluoride-containing gel-treated, 4) F varnish-treated, and 5) polydopamine- and fluoride ion-coated enamels. Vickers hardness number (VHN), morphology, and fluoride contents of the specimens were measured before and after the pH-cycling regimen. RESULTS: Polydopamine- and fluoride ion-coated enamels showed the highest fluoride content and lowest VHN reduction among the samples. The fluoride content of the polydopamine/fluoride ion (PD/F)-coated enamel was increased to 182 ± 6.6%, which was far higher than that of the uncoated enamel (112.3 ± 32.8%, P < 0.05). The changes in the VHN values (ΔVHN) of PD/F-coated enamel substrates showed a slight reduction in the VHN (-3.6%, P < 0.05), which was far lower than that in the control group (-18.9%, P < 0.05). In addition, scanning electron microscopy clearly supported the effect of polydopamine- and fluoride ion-coatings on the remineralization of enamel specimens. CONCLUSION: Our findings suggest that one-pot treatments with polydopamine and fluoride ions could significantly enhance remineralization by inhibiting enamel demineralization through the prolonged retention of fluoride ions.

Nasolacrimal duct obstruction after maxillary orthognathic surgery.

PURPOSE: To report cases of nasolacrimal duct obstruction (NLDO) after maxillary orthognathic surgery. MATERIALS AND METHODS: The authors reviewed the clinical manifestations, dacryocystographic images, and orbital computed tomographic scans of 10 patients who were diagnosed with NLDO after undergoing maxillary orthognathic surgery. RESULTS: Six of the 10 patients (60%) complained of epiphora immediately after the surgery. Bilateral (n = 2, 20%) or unilateral (n = 8, 80%) NLDO occurred in all patients involved in the study. Twelve eyes of 10 patients were examined, and dacryocystography showed that the obstruction was present in the distal ostium in 7 eyes (58.3%), the junction between the sac and duct in 3 eyes (25%), and the common canaliculus in 2 eyes (16.7%). Computed tomographic scans of all subjects showed that mucosal swelling and congestion around the distal NLD opening narrowed the space between the lateral nasal wall and the inferior turbinate of the affected side. Dacryocystorhinostomy was performed in 9 eyes (8 patients), with a success rate of 100%. CONCLUSIONS: The distal to proximal portion of the NLD can become obstructed after maxillary orthognathic surgery. This obstruction seems to be caused by secondary inflammatory changes associated with an indirect injury of the NLD. Therefore, clinicians should be aware of the possibility of NLDO after orthognathic surgery, which can be treated successfully with dacryocystorhinostomy.

Concentration-dependent collateral sensitivity of cisplatin-resistant gastric cancer cell sublines.

The cisplatin-resistant gastric cancer cell sublines, SNU-601/Cis2 and /Cis10, were 49 and >530 times more resistant to cisplatin, respectively, compared with the drug-sensitive cells, SNU-601/WT. The SNU-601/Cis2 showed cross-resistance to carboplatin, heptaplatin, doxorubicin, mitomycin C, and 5-fluorouracil compared with the SNU-601/WT whereas the SNU-601/Cis10 displayed collateral sensitivity to these drugs with the exception of cisplatin compared with the SNU-601/Cis2, suggesting that the cross-resistance and collateral sensitivity of cisplatin-resistant gastric cancer cells are dependent upon cisplatin concentrations. Altered expression of the antioxidant and transporter genes (metallothionein, catalase, superoxide dismutases, P-glycoprotein, and the breast cancer resistance protein) was involved in these phenotypes of the cisplatin-resistant gastric cancer cell lines.

Fas (Apo-1/CD95) and Fas ligand interaction between gastric cancer cells and immune cells.

BACKGROUND AND AIMS: It has been proposed that the expression of Fas ligand (Fas L) in tumors may play an important role in immune escape. This study was undertaken to test a 'counterattack' theory as a mechanism of immune escape in gastric carcinoma. METHODS: Expression of Fas and Fas L was examined in the human gastric cancer cell lines using reverse transcription-polymerase chain reaction. Cytotoxicity was determined by the MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide] assay. Apoptosis of target Jurkat cells was examined after coculture with the effector gastric cancer cells in vitro. Immunohistochemical staining was performed for the detection of Fas and FasL in tumor-infiltrating lymphocytes (TIL) and gastric cancer cells in vivo. Apoptosis was detected by terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick-end labeling (TUNEL) method in vitro and in vivo. RESULTS: Fas and FasL mRNA were found to be differentially expressed in gastric cancer cell lines. The coculture experiment showed that apoptosis of Jurkat was induced by a FasL-overexpressing effector gastric cell SNU-484. In a Fas-expressing gastric cell SNU-638, Fas expression was upregulated by the treatment of gamma-interferon in a time- and concentration-dependent manner. SNU-638 treated with gamma-interferon was more sensitive to anti-Fas antibody-mediated cytotoxicity than was the control cell line, suggesting an increase of functional Fas in gastric cancer cells. The expression of FasL in gastric cancer cells and of Fas in apoptotic TIL was also detected in vivo. CONCLUSION: The data indicate that the FasL expression of gastric cancer cells supports a 'counterattack theory' in gastric cancer cells and that the upregulation of Fas by IFN-gamma in SNU-638 may accelerate the apoptosis pathway through the Fas and FasL interaction between gastric cancer cells and immune cells. This result is supported by the expression of FasL in gastric cancer cells and apoptotic TIL in vivo. It is implicated that the different biological behaviors of gastric cancer cells could be at least in part explained by Fas and FasL interaction with immune cells.