BACKGROUND: The rupture of syndesmotic ligaments is treated with a screw fixation as the gold standard. An alternative is the stabilization with a TightRope®. A couple of studies investigated the different clinical outcome and some even looked at the stability in the joint, but none of them examined the occurring pressure after fixation. OBJECTIVE: Is there a difference in pressure inside the distal tibiofibular joint between a screw fixation and a TightRope®? Does the contact area differ in these two treatment options? METHODS: This biomechanical study aimed to investigate the differences in fixation of the injured syndesmotic ligaments by using a fixation with one quadricortical screw versus singular TightRope® both implanted 1 cm above the joint. By using 12 adult lower leg cadaveric specimens and pressure recording sensor, we recorded the pressure across the distal tibiofibular joint. Additionally we measured the contact surface area across the joint. RESULTS: The mean of the pressure across the distal tibiofibular joint from the start of the insertion of the fixation device to the complete fixation was 0.05 Pascal for the TightRope® and 0.1 for the screw (P= 0.016). The mean of the maximum pressure across the joint (after completion of fixation and releasing the reduction clamp) was 1.750 mega Pascal with the screw fixation and 0.540 mega Pascal with TightRope® (P= 0.008). The mean of the measured contact area of the distal tibiofibular joint after fixation was 250 mm2 in the TightRope® group and of 355 mm2 in the screw fixation (P= 0.123). CONCLUSIONS: The screw fixation is stronger and provides a larger surface contact area, which leads us to the conclusion that it provides a better stability in the joint. While previous clinical studies did not show significant clinical difference between the two methods of fixation, the biomechanical construct varied. Long term clinical studies are required to establish whether this biomechanical distinction will contribute to various clinical outcomes.
The pro-inflammatory adipokine resistin induces a phenotypic switch of vascular smooth muscle cells (VSMC), a process decisive for atherosclerosis, including morphological changes, increased synthetic activity, proliferation and migration. The guanine-exchange factor ARNO (Cytohesin-2) has been shown to be important for morphological changes and migration of other cell types. In this study we dissected the role of ARNO in resistin induced VSMC phenotypic switching and signalling. Firstly, treatment with the cytohesin inhibitor Secin H3 prevented the resistin mediated induction of morphological changes in VSMC. Secondly, Secin H3 treatment as well as expression of an inactive ARNO (EK) reduced resistin induced VSMC synthetic activity, as assessed by matrix metalloproteinase 2 (MMP-2) expression, as well as the migration into a wound in vitro compared to ARNO WT expression. Thirdly, we found ARNO to influence MMP-2 expression and migration via activation of p38 MAPK and the JNK/AP-1 pathway. Interestingly, these processes were shown to be dependent on the binding of PIP 3 , as mutation of the ARNO PH-domain inhibited VSMC migration, MMP-2 expression as well as p38 MAPK and JNK signalling. Thus, we demonstrate that ARNO is an important link in resistin dependent cell signalling leading to morphological changes, MMP-2 production and migration of VSMC.Resistin is an adipokine, which is mainly expressed in peripheral blood mononuclear cells and macrophages 1,2 . Resistin levels were first found to be enhanced in serum of diabetic as well as obese mice 3 . In human, increased serum levels of resistin in diabetic and obese patients 4-6 was furthermore shown to correlate with the accumulation of metabolic syndrome factors in type 2 diabetes 7 as well as with other inflammatory diseases, such as atherosclerosis, rheumatic disease and sepsis 2,8 . As all these mentioned pathophysiological conditions are associated with vascular inflammation and thus an elevated risk of cardiovascular disease 9-11 , resistin has gained increasing interest as a potential biomarker 12 and target of therapeutic interventions 8 in the context of vascular inflammation and cardiovascular disease.Upon stimulation with inflammatory cytokines or adipokines, vascular smooth muscle cells (VSMC) undergo a phenotypic switch from a quiescent differentiated contractile phenotype to a proliferative, migratory and synthetic dedifferentiated one 13 . The phenotypic changes of VSMC contribute to the development of atherosclerosis 14 . During this process VSMC undergo morphological changes and downregulate proteins determining the contractile phenotype, such as smooth muscle (SM) α-Actin or SM myosin heavy chain, and instead upregulate genes such as metalloproteinases (MMP), characteristic for an increased synthetic activity, important for the invasive process, i.e. proliferation and migration 13 . VSMC migration is a complex process involving remodelling of the cytoskeleton, integrins regulating adhesion by interaction with extracellular matrix (ECM) proteins ...
Due to their immunomodulatory and regenerative capacity, human bone marrow-derived mesenchymal stem cells (hBMSCs) are promising in the treatment of patients suffering from polytrauma. However, few studies look at the effects of sera from polytraumatized patients on hBMSCs. The aim of this study was to explore changes in hBMSC properties in response to serum from polytrauma patients taken at different time points after the trauma incident. For this, sera from 84 patients with polytrauma (collected between 2010 and 2020 in our department) were used. In order to test the differential influence on hBMSC, sera from the 1st (D1), 5th (D5), and 10th day (D10) after polytrauma were pooled, respectively. As a control, sera from three healthy donors (HS), matched with respect to age and gender to the polytrauma group, were collected. Furthermore, hBMSCs from four healthy donors were used in the experiments. The pooled sera of HS, D1, D5, and D10 were analyzed by multicytokine array for pro-/anti-inflammatory cytokines. Furthermore, the influence of the different sera on hBMSCs with respect to cell proliferation, colony forming unit-fibroblast (CFU-F) assay, cell viability, cytotoxicity, cell migration, and osteogenic and chondrogenic differentiation was analyzed. The results showed that D5 serum significantly reduced hBMSC cell proliferation capacity compared with HS and increased the proportion of dead cells compared with D1. However, the frequency of CFU-F was not reduced in polytrauma groups compared with HS, as well as the other parameters. The serological effect of polytrauma on hBMSCs was related to the time after trauma. It is disadvantageous to use BMSCs in polytraumatized patients at least until the fifth day after polytrauma as obvious cytological changes could be found at that time point. However, it is promising to use hBMSCs to treat polytrauma after five days, combined with the concept of “Damage Control Orthopedics” (DCO).
Purpose Smaller posterior acetabular walls have been shown to independently influence the risk for bipolar hip dislocation. We asked whether differences would also be observed in patients with traumatic posterior hip dislocation with and without posterior wall fractures. Methods Between 2012 and 2020 we observed 67 traumatic posterior hip dislocations. Of these, 43 traumatic posterior hip dislocations in 41 patients met the inclusion criteria. Eighteen dislocations were excluded with an acetabular fracture other than posterior wall fracture and six dislocations had insufficient computed tomography (CT) data. The mean age was 41 ± 11 years, 32 males and nine females. We observed 26 traumatic hip dislocations with posterior wall fractures and 17 without. All patients underwent polytrauma CT scans and postoperative/postinterventional pelvic CT scans. On axial CT-scans, posterior wall determining angles were measured. Results Patients with posterior wall fractures were not significantly older than patients without posterior wall fractures (42 ± 12 vs. 38 ± 10 years; p = 0.17). Patients without posterior wall fractures had significantly smaller posterior acetabular sector angles (84° ± 10°) than did patients with posterior wall fractures (105° ± 12°) (p < 0.01; OR 1.178). Likewise, the posterior wall angle was significantly smaller in patients without posterior wall fracture (62° ± 9°) than in those with posterior wall fractures (71° ± 8°) (p < 0.01; OR 1.141). Conclusion Both posterior acetabular sector angle and posterior wall angle are independent factors determining the posterior wall fracture morphology in patients with traumatic posterior hip dislocation. Age and the observed trauma mechanism did not differentiate between traumatic posterior hip dislocations with and without posterior wall fractures.
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