Risk factors for redislocation of chronic Monteggia fracture-dislocation in children after reconstruction surgery.

INTRODUCTION: Monteggia fracture-dislocation refers to traumatic ulnar fractures and dislocation of the radial head, which is one of the most frequently missed injuries, especially in children. The most widespread attitude towards chronic Monteggia lesion is the open reduction of the radial head associated with ulnar osteotomy with or without annular ligament reconstruction. Our study aimed to analyze the risk factors for redislocation after surgical management of chronic Monteggia lesion and the benefits of annular ligament reconstruction and radiocapitellar pinning in paediatric. MATERIALS AND METHODS: We retrospectively reviewed patients treated with reconstruction surgery for chronic Monteggia fracture-dislocation in our department between 2005 and 2017, with a minimum two years' follow-up. The reconstruction surgery included ulnar osteotomy performed in all patients, annular ligament repair or reconstruction or fixation of radiocapitellar joint, or radial osteotomy in some patients. We collected the related clinical data and evaluated the risk factors of redislocation using logistic regression analyses and a two-piecewise linear regression model with a smoothing function, after reconstruction. RESULTS: Throughout a mean six years' follow-up (range, 2-14 years), 62 patients (42 males, 20 females; average age 6.49 years range, 2-13 years) were reviewed. Of the radiocapitellar joints, 16.1% was noted to have redislocation. Univariate risk analysis showed age, time from injury to surgery, and radial osteotomy were risk factors for a recurrent radiocapitellar redislocation. Time from injury to surgery was found to be independent predictor of redislocation in multivariate analysis. However, there were significant nonlinear associations between time from injury to surgery and redislocation in multivariate logistic regression analysis after multivariate adjustment (p for nonlinear = 0.023). Every one month increase was associated with a 1.37-fold increase in redislocation, in participants within one year after injury. CONCLUSION: In conclusion, the surgery of chronic Monteggia fracture-dislocation should be done as quickly as possible within one year after injury. Associated annular ligament reconstruction or fixation of radiocapitellar joint does not seem to be helpful.

The effect of temporary hemiepiphysiodesis in the treatment of skeleton immature posttraumatic genu angular deformity: a retrospective study of 27 cases.

BACKGROUND: The purpose of this study was to evaluate the effect, rate of angular correction, and complications of temporary hemiepiphysiodesis (TH) in the treatment of skeleton immature posttraumatic genu angular deformity. METHODS: We retrospectively reviewed the records of 27 patients undergoing temporary hemiepiphysiodesis for the management of posttraumatic genu angular deformity. Based on the data from these patients, the rate of correction, effect of correction, length of the lower limbs, and complications were used as the outcome measures. RESULTS: Outcome measurements were obtained from a chart review of medical records that included information about clinical evaluations. Fifteen boys and 12 girls, with an average age of 6.3 years, were included in the study. The average follow-up was 3.8 years (range, 1.9 to 5.9 years) after surgery. Complete correction was obtained in 24 patients, while partial correction was obtained in 3 patients. The mean rate of angular correction was 8.41°/year in distal femur and 15.19°/year in proximal tibia. One patient had recurrence of genu valgum. No leg length discrepancy was found in our patients. CONCLUSION: Temporary hemiepiphysiodesis is a simple, effective, reliable, and reproducible method for the treatment of posttraumatic genu angular deformity, with fewer complications than osteotomy. Nevertheless, it is important to follow the rebound patient closely until skeletal maturity in our future work.

Effect of Hemiepiphysiodesis on the Growth Plate: The Histopathological Changes and Mechanism Exploration of Recurrence in Mini Pig Model.

PURPOSE: Hemiepiphysiodesis has been widely used to correct angular deformity of long bone in immature patients. However, there is a limited knowledge about the biomechanical effect of this technique on the histopathological changes of the growth plate and the mechanism of recurrence of malformation after implant removal. We aimed to evaluate the biomechanical effect of hemiepiphysiodesis on the histopathological changes of the growth plate and the mechanism of recurrence of malformation after implant removal in Bama miniature pigs, and to explore the role of asymmetric stress during this procedure. METHODS: Eight 3-month-old male Bama miniature pigs sustained surgeries on the bilateral medial hind leg proximal tibia as the intervention group (n=16), and four pigs sustained bilateral sham surgeries as the control (n=8). In the 18th week after surgeries, hardware was removed in the unilateral leg of each animal in the intervention group. In the 24th week of the study, all animals were euthanized. A total of 24 samples were obtained and stained with H&E, TUNEL, and immunohistochemistry. Sixteen samples in the intervention group were divided into two subgroups. The tibias without an implant were included in the implant removal group (IR group), while the tibias with an implant were included in the implant persist group (IP group). The proximal tibia specimens were divided into 3 equidistant parts from medial to lateral, named as area A, area B, and area C, respectively. The change of thickness of growth plates, chondral apoptosis index, and the expression of Caspase-3, Caspase-9, CHOP, and P65 were compared. RESULTS: H&E staining showed the thickness of growth plate to be varied in different areas. In the IP group, the thickness of growth plate in areas A and B was statistically significantly thinner than that in area C (p<0.05). In the IR group, the thickness of growth plate in areas A and B was statistically significantly thicker than that in area C (p<0.05). TUNEL staining showed that the apoptosis rate increased significantly after hemiepiphysiodesis and declined after implant removal (p<0.05). Immunohistochemical staining suggested that the expression of Caspase-3, Caspase-9, P65, and CHOP protein was upregulated in the experimental group and downregulated after implant removal. CONCLUSION: The thickness parameter of the growth plate changes with asymmetric pressure. When the pressure is relieved, the recurrence of malformation is related to the thickening of the growth plate.

Leptin induces the apoptosis of chondrocytes in an in vitro model of osteoarthritis via the JAK2­STAT3 signaling pathway.

Emerging data has suggested a high prevalence of osteoarthritis (OA) among obese people. As an important adipokine secreted by white adipose tissue, leptin may be a key mediator in the progression of OA. Leptin exerts a catabolic effect on OA cartilage by increasing the production of metalloproteinase (MMP) enzymes, and contributes to apoptosis in chondrocytes. The current study aimed to explore the role of leptin on the apoptosis of chondrocytes in OA, and its underlying mechanisms. In the in vitro model of OA used in the present study, administration of exogenous leptin induced the generation of reactive oxygen species (ROS) and apoptosis in chondrocytes. It has been demonstrated that leptin is associated with the pathogenesis of OA via the Janus kinase 2 (JAK2)­signal transducer and activator of transcription 3 (STAT3) signaling pathway, and data gathered in the present study demonstrated that suppression of this signaling pathway using a JAK2 inhibitor, AG490, significantly ameliorated leptin­induced apoptosis in damaged chondrocytes in vitro, and reduced the generation of ROS. Furthermore, the protein expression levels of MMP­13 and B­cell lymphoma 2­associated X protein were downregulated in the AG490­treated group. The results of the present study may provide insight into the underlying molecular mechanism by which leptin induces apoptosis in chondrocytes. These findings indicated the importance of leptin as a therapeutic target for the treatment of OA in the overweight population.