Camouflage treatment for skeletal Class III patient with facial asymmetry using customized bracket based on CAD/CAM virtual orthodontic system.

When considering camouflage orthodontic treatment for Class III malocclusion with skeletal facial asymmetry, it is crucial to preserve the favorable compensated posterior occlusion. Once the inclination of the compensated occlusion is changed during orthodontic treatment, unstable occlusion, such as crossbite or scissor bite may occur. A 23-year-old female patient had anterior spacing with Class III malocclusion and a mandibular asymmetry. A nonsurgical approach was adopted. The treatment objectives were to establish a Class I molar relationship with compensated inclination of the posterior dentition and to correct the midline deviation. To achieve these goals, the computer-aided design/computer-aided manufacturing (CAD/CAM) orthodontic system plus customized brackets was applied, and miniscrews were used to distalize the left mandibular dentition for midline correction. The results suggested that the CAD/CAM-based customized brackets can be efficiently used in camouflage treatment to achieve a correct final occlusion.

Similarity index for intuitive assessment of three-dimensional facial asymmetry.

Evaluation of facial asymmetry generally involves landmark-based analyses that cannot intuitively assess differences in three-dimensional (3D) stereoscopic structures between deviation and non-deviation sides. This study tested a newly developed similarity index that uses a mirroring technique to intuitively evaluate 3D mandibular asymmetry, and characterised the resulting lower facial soft tissue asymmetry. The similarity index was used to evaluate asymmetry before and after surgery in 46 adult patients (27 men, 19 women; age, 22 ± 4.8 years) with skeletal Class III malocclusion and facial asymmetry who underwent conventional bimaxillary orthognathic surgery. Relative to the midsagittal plane used as the reference plane, the non-overlapping volume of the mandible significantly decreased, and the similarity index significantly increased after surgery. Similarity indexes of the mandible and lower facial soft tissue were strongly negatively correlated with non-overlapping volumes of each measurement. Differences in bilateral hemi-mandibular and hemi-lower facial soft tissue surface and volume measurements before surgery were significantly negatively correlated with similarity indexes of the mandible before and after surgery. This newly developed similarity index and non-overlapping volume using a mirroring technique can easily and intuitively evaluate overall 3D morphological discrepancies, especially 3D mandibular asymmetry, before and after surgery in skeletal Class III patients with facial asymmetry.

Diagnosis and Surgical Outcomes of Facial Asymmetry According to the Occlusal Cant and Menton Deviation.

PURPOSE: Morphologic differences and surgical outcomes were compared between the ipsilateral type of facial asymmetry, in which the menton deviates to the side of the upward frontal occlusal plane (FOP) cant (FOPUP), and the contralateral type, in which the menton deviates to the side of the downward FOP cant (FOPDOWN), by using cone beam computed tomography (CBCT) images. MATERIALS AND METHODS: This retrospective study included consecutive patients with skeletal Class III malocclusion and facial asymmetry who had undergone bimaxillary orthognathic surgery and serial CBCT before, 1 month after, and 1 year after surgery. CBCT images were reconstructed and analyzed for predictor (group and timing) and outcome (CBCT measurements over time) variables. The data were analyzed using independent t tests and paired t tests. RESULTS: The contralateral group (n = 12) was selected first; the ipsilateral group (n = 12) was selected by matching age, gender, and degree of FOP cant with those of the contralateral group. Before surgery, in the ipsilateral group, the ramal length was longer on the nondeviated (N-Dev) side than on the deviated (Dev) side (P < .05) whereas the mandibular body length showed no significant difference (P > .05). In the contralateral group, the ramal length was longer on the Dev side (P < .05) whereas the mandibular body length was longer on the N-Dev side (P < .01). One year after surgery, most measurements were corrected symmetrically in both groups (P > .05); however, the hemi-lower facial area remained asymmetrical in the contralateral group (P < .05). CONCLUSIONS: Differences in ramal lengths in the ipsilateral group and mandibular body lengths in the contralateral group between the Dev and N-Dev sides seemed to be the main cause of facial asymmetry. Although facial asymmetry improved after surgery in both groups, asymmetry in the soft tissue remained in the contralateral group 1 year after surgery.

Anti-cancer effect of N-(3,5-bis(trifluoromethyl)phenyl)-5-chloro-2,3-dihydronaphtho[1,2-b]furan-2-carboxamide, a novel synthetic compound.

Naphthofuran compounds have been known to regulate HNF 4α which is associated with proliferation, progression and metastasis of HCC. In this study, we investigated whether N-(3,5-bis(trifluoromethyl)phenyl)-5-chloro-2,3-dihydronaphtho[1,2-b]furan-2-carboxamide (NHDC), a novel synthetic naphthofuran compound inhibits liver tumor growth through activation of HNF 4α. Treatment with different concentrations (1-10.8 µM) of NHDC for various periods (0-72 h) inhibited liver cancer cells (HepG2, Hep3B) growth as well as colony formation followed by induction of apoptosis in a concentration dependent manner. NHDC also induced expression of the apoptosis regulating genes as well as inhibiting the action of STAT3. These inhibitory effects were associated with enhancement of expression and DNA binding activity of HNF 4α. In vivo study confirmed that liver tumor growth was prevented with NHDC (5 mg/kg), and its effect was also related with inhibition of STAT3 pathway through enhancement of expression and DNA binding activity of HNF 4α. Moreover, siRNA of HNF 4α abolished NHDC-induced cell growth inhibition as well as DNA binding activity and phosphorylation of STAT3. Pull down assay docking prediction analysis proved that NHDC directly binds to hydrophobic fatty acid ligand binding site of HNF 4α. A novel naphthofuran compound, NHDC inhibited liver tumor growth by inactivating of STAT3 through direct biding to HNF 4α.

Deficiency of C-C chemokine receptor 5 suppresses tumor development via inactivation of NF-κB and inhibition of monocyte chemoattractant protein-1 in urethane-induced lung tumor model.

To evaluate the significance of C-C chemokine receptor type 5 (CCR5) in lung tumor development, we compared carcinogen-induced tumor growth in CCR5 knockout (CCR5(-/-)) mice and wild-type (CCR5(+/+)) mice. CCR5(-/-) mice showed reduced urethane (1g/kg)-induced tumor incidence when compared with those of CCR5(+/+) mice. We investigated the activation of nuclear factor-kappaB/STAT3 since these are implicated transcription factors in the regulation of genes involving tumor growth. Significant inhibition of DNA-binding activity of nuclear factor-kappaB and STAT3, and the translocation of p50 and p65 into the nucleus and the phosphorylation of IĸB were found in the lungs of CCR5(-/-) mice compared with the lungs of CCR5(+/+) mice. Expression of apoptotic protein such as cleaved caspase-3, cleaved PARP and Bax was elevated, whereas the expression levels of survival protein such as Bcl-2 and cIAP1 was decreased in the lungs of CCR5(-/-) mice. Interestingly, we found that the level of monocyte chemoattractant protein-1 (MCP-1), a tumor growth-promoting cytokine, was significantly reduced in the lung tumor tissue and blood of CCR5(-/-) mice compared with the level in CCR5(+/+) mice. In addition, CCR5 small interfering RNA (siRNA) and inhibitor of MCP-1 blocked lung cancer cell growth, which was abolished by the addition of MCP-1 protein in cultured lung cancer cells. Moreover, inactivation of CD8(+) cytotoxic T cell and dendritic cells was significantly increased in the blood, lung tumors and spleens of CCR5(-/-) mice compared with that of CCR5(+/+) mice. Therefore, these results showed that CCR5 deficiency suppressed lung tumor development through the inhibition of nuclear factor-kappaB/STAT3 pathways and the downregulation of MCP-1 in the carcinogen-induced lung tumor model.