Evaluation of Postoperative Stability After Open Reduction and Internal Fixation of Zygomaticomaxillary Complex Fractures Using Cone Beam Computed Tomography Analysis.

The aim of this study was to evaluate whether the amount of fracture displacement affects postoperative stability of isolated zygomaticomaxillary complex fractures and to determine whether the 1-point fixation method is as stable as 2- or 3-point fixation methods. The authors investigated 14 patients with 1-point fixation in the zygomaticomaxillary area (group A), 14 patients with 2-point fixation in the zygomaticomaxillary and frontozygomatic area (group B), and 13 patients with 3-point fixation in the zygomaticomaxillary, frontozygomatic, and infraorbital rim area (group C). Stability of the reduced zygomaticomaxillary complex was assessed by comparing immediate postoperative cone beam computed tomography images with those obtained at least 3 months later. Preoperatively, the total mean displacement was 3.79 ±â€Š1.36 mm in group A, 3.43 ±â€Š0.89 mm in group B, and 3.86 ±â€Š1.57 mm in group C. The total postoperative orbital and screw changes were 0.91 ±â€Š0.18 and 0.72 ±â€Š0.08 mm, respectively, in group A; 0.92 ±â€Š0.19 and 0.68 ±â€Š0.09 mm, respectively, in group B; and 0.91 ±â€Š0.11 and 0.66 ±â€Š0.10 mm, respectively, in group C. There were no significant relationships between postoperative stability and amount of fracture displacement in any of the 3 groups, or between the 3 groups (P > 0.05). There was little difference in postoperative stability between the 3 groups. Hence, the amount of displacement is not a very important consideration when deciding the fixation method, including the number and location of miniplates applied for fixation.

Transient ischemia-induced expression and changes of tyrosine kinase A in the hippocampal dentate gyrus of the gerbil.

The present study examined ischemia-related changes in tyrosine kinase A (trkA) immunoreactivity and its protein content in the dentate gyrus after 5 min of transient forebrain ischemia in gerbils. One day after ischemic insult, cresyl violet-positive polymorphic cells showed ischemic degeneration. The ischemia-induced changes in trkA immunoreactivity were found in the polymorphic layer (PL) and granule cell layer (GCL) of the dentate gyrus. In the sham-operated group, trkA immunoreactivity in the dentate gyrus was very weak. From 30 min after ischemia, trkA immunoreactivity was increased in the dentate gyrus and peaked in the dentate gyrus at 12 h after ischemia-reperfusion. Thereafter, trkA immunoreactivity was decreased time-dependently after ischemia-reperfusion. Four days after ischemic insult, trkA immunoreactivity was similar to that of the sham-operated group. In addition, it was found that ischemia-related changes in trkA protein content were similar to the immunohistochemical changes. These results suggest that the chronological changes of trkA in the dentate gyrus after transient forebrain ischemia may be associated with ischemic damage in polymorphic cells of the dentate gyrus.

Ischemia-related changes in galanin expression in the dentate hilar region after transient forebrain ischemia in gerbils.

Although galanin (GAL) protects hippocampal neurons from ischemic damage, no study has examined ischemia-related changes in endogenous GAL in the hippocampal dentate gyrus. We investigated the chronological changes of GAL, well-known as the potassium channel opener, expression in the dentate gyrus at various times after 5 min of transient forebrain ischemia in gerbils. A few GAL-immunoreactive (IR) neurons were found in the polymorphic layer of the sham-operated group. Three hours after ischemia-reperfusion, the pattern of GAL immunoreactivity was similar to that of the sham-operated group and the number of GAL-IR neurons and immunoreactivity were highest 12 h after ischemic insult. At this time, GAL-IR neurons in the polymorphic layer showed strong GAL immunoreactivity. Thereafter, GAL-IR neurons and immunoreactivity significantly decreased in the dentate hilar region. Four days after ischemic insult, GAL-IR neurons were not detectable. In addition, the results of a Western blot study showed a pattern of GAL expression similar to the immunohistochemical changes. GAL protein content also was highest 12 h after ischemia. In conclusion, the increased expression of endogenous GAL in the dentate gyrus after ischemia is related to response to the ischemic damage.