The aims of this study were to determine the reaction of the craniofacial bones on the protraction force transferred to the maxillary body, and whether or not the midpalatal suture had opened during skeletal Class III treatment. A computerized tomograph was obtained from a dry skull with a normal occlusion to construct a three-dimensional finite-element model (3D.FEM) of the craniofacial bones and the maxillary teeth to simulate actual bone reactions. A protraction force of 500 g was applied at the first premolar region, directed 20 degrees inferior to the occlusal plane. The displacement and the stress distribution of the craniofacial bones and sutures were then calculated using the ANSYS 5.3 program dividing the analysis into two simulations, based on whether or not the midpalatal suture was opened. The results showed that there was less compressive stress and greater tensile stress in the circumaxillary suture areas when the midpalatal suture was opened. The amount of displacement and deformation when the midpalatal suture was opened also demonstrated a decrease in upward-forward rotation of the maxilla and zygomatic arch and greater amounts of displacement in the frontal, vertical, and lateral directions compared with no opening of the midpalatal suture. Analysis of these results showed that maxillary protraction produce similar changes to normal downward and forward growth of the maxilla and was achieved with accompanying opening of the midpalatal suture.
Intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1) play key roles in the initiation of vascular inflammation. In this study, we explored whether sulforaphane, a dietary phytochemical, can inhibit the expression of ICAM-1 and VCAM-1 in human umbilical vein endothelial cells (HUVEC) stimulated with lipopolysaccharide (LPS), and the mechanisms involved. Sulforaphane prevented the LPS-mediated increase in ICAM-1 and VCAM-1 expression, (P < 0.01) in HUVEC. Sulforaphane also prevented the LPS-mediated increase in the phosphorylation of signal transducer and activator of transcription 3 (STAT3) (P < 0.01). Stattic, a STAT3 inhibitor, reduced the LPS-induced expression of ICAM-1 and VCAM-1, and STAT3 phosphorylation (P < 0.01). STAT3 small interfering RNA treatment reduced the LPS-induced expression of ICAM-1, VCAM-1, and STAT3 (P < 0.01). Sulforaphane reduced LPS-mediated THP-1 monocyte adhesion to HUVEC (P < 0.01). In C57BL/6 mice, injection of LPS increased aortic ICAM-1 and VCAM-1 expression, and this effect was prevented by sulforaphane. These data provide insight into the mechanism through which sulforaphane partly reduces the expression of ICAM-1 and VCAM-1 on the vascular wall by inhibiting STAT3 phosphorylation.
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