Unstable external-rotation type ankle fractures with concomitant syndesmosis injury commonly occur. Syndesmosis screw fixation has long been regarded as a reference standard treatment for syndesmosis injury. However, its complications and biomechanical disadvantages have become controversial; thus, we designed a novel elastic syndesmosis hook plate (ESHP) that combines the features of both rigidity and flexibility. The purpose of the present study was to introduce this new method and compare its clinical outcomes with those of routine screw fixation. We randomized 25 patients to the screw fixation group and ESHP group. The average follow-up period was 12 months. The clinical outcomes included malreduction or loss of reduction, overall complications, and function. During the follow-up period, 3 cases (25%) of malreduction were found in screw fixation group on postoperative computed tomography. In the ESHP group, only 1 patient (7.69%) had a narrowed anterior gap between the distal tibia and fibula. However, the difference in the malreduction rate between the 2 groups was not significant statistically (p = .32). The overall complication rate in the ESHP group was lower than that in the screw group, although no significant differences were found between the 2 groups. The mean visual analog scale scores in the ESHP and screw groups were 1.46 ± 1.33 and 2.42 ± 2.07, respectively. The average dorsiflexion range of motion in both groups was satisfactory (14.77° versus 12.83°; p = .16). However, a statistically significant difference was found in the plantarflexion range of motion between the 2 groups (p < .05). In addition, the ESHP group had an earlier time to return to work (p < .05). The ESHP fixation construct can stably fix syndesmosis, retain the physiologic micromotion function of the syndesmosis, and results in fewer complications compared with routine syndesmosis screw fixation for syndesmotic instability. In conclusion, our results have shown ESHP to be a viable method for treatment of syndesmosis instability.
Autophagy, which is a mechanism for the turnover of intracellular molecules and organelles, protects cells during stress responses; however, the role of autophagy in the stages of bone fracture remains to be elucidated. The aim of the present study was to investigate the process of autophagy in bone tissue at different time-points after fracture. A femur fracture model was established in male adult Wistar rats via surgery. The protein expression of microtubule-associated protein II light chain 3 (LC3-II) was analyzed in a femur fracture (experimental) group and a sham-surgery group using immunofluorescence. The protein expression of proliferating cell nuclear antigen (PCNA) was used to investigate the cell proliferation in bone tissue following fracture via immunohistochemical analysis. The correlation between cell proliferation and autophagy was analyzed using linear regression. LC3-II protein was constitutively expressed in the sham-surgery group; however, compared with the expression in the sham-surgery group, the LC3-II expression in the experimental group was significantly increased at each time-point (P<0.05). Similarly, immunohistochemistry revealed that the number of PCNA-positive cells in each section was significantly increased following fracture injury (P<0.01). A comparison of the LC3-II- and PCNA-positive rates in the experimental group rats at each time-point revealed a linear correlation (R2=0.43, P<0.01). In conclusion, surgically induced fracture in rats is associated with an increase in LC3-II and PCNA protein expression during the initial stages of fracture injury, and a correlation exists between the expression of the two proteins. These results suggest that potential treatment aimed at improving fracture healing should target the process of autophagy.
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