Prebending of osteosynthesis plate using 3D printed models to treat symptomatic os acromiale and acromial fracture

Abstract Background A symptomatic os acromiale can lead to impingement syndrome and rotator cuff tendinopathy. An acromion fracture is often part of a more complex scapular trauma that needs stabilisation. Methods We developed a new technique using a three-dimensional (3D) model and a distal clavicle reconstruction plate to treat os acromiale and acromion fractures. Our hypothesis was that such an approach would be a useful addition to the existing techniques. First, a 3D model of the acromion was printed, then an osteosynthesis plate was pre-bent to fit the exact shape and curve of the acromion. We tested this technique and present reports on five patients, three with os acromiales and two with acromial fractures. We followed these patients during their rehabilitation and evaluated them using the Constant–Murley and the Disabilities of the Arm, Shoulder and Hand scores. Results In every case the fracture or non-union healed. If the surgery was performed before additional damage (such as an impingement syndrome) occurred, we saw that the patient’s pain completely disappeared. This new technique also has other advantages because the surgeon can prepare the entire operation in advance, which reduces the duration of surgery. Another advantage of using a 3D model is that it can also be used to inform the patient and the surgical team about the planned operation. Conclusion This new technique using a preoperative patient-customized plate is a good alternative for use in open reduction and internal fixation, particularly if the patient has no other conditions

The Impact of Advanced Glycation End-Products (AGEs) on Proliferation and Apoptosis of Primary Stem Cells: A Systematic Review

Stem cell-based regenerative therapies hold great promises to treat a wide spectrum of diseases. However, stem cell engraftment and survival are still challenging due to an unfavorable transplantation environment. Advanced glycation end-products (AGEs) can contribute to the generation of these harmful conditions. AGEs are a heterogeneous group of glycated products, nonenzymatically formed when proteins and/or lipids become glycated and oxidized. Our typical Western diet as well as cigarettes contain high AGEs content. AGEs are also endogenously formed in our body and accumulate with senescence and in pathological situations. Whether AGEs have an impact on stem cell viability in regenerative medicine remains unclear, and research on the effect of AGEs on stem cell proliferation and apoptosis is still ongoing. Therefore, this systematic review provides a clear overview of the effects of glycated proteins on cell viability in various types of primary isolated stem cells used in regenerative medicine

Glycolaldehyde-derived high-molecular-weight advanced glycation end-products induce cardiac dysfunction through structural and functional remodeling of cardiomyocytes

Background/Aims: High-molecular-weight advanced glycation end-products (HMW-AGEs) are abundantly present in our Western diet. There is growing evidence reporting that HMW-AGEs contribute to the development of cardiovascular dysfunction in vivo, next to the well-known low-molecular-weight AGEs. The goal of our study is to assess the ultrastructure and function of cardiomyocytes after chronic exposure to HMW-AGEs. A better understanding of underlying mechanisms is essential to create new opportunities for further research on the specific role of HMW-AGEs in the development and progression of cardiovascular diseases. Methods: Adult male rats were randomly assigned to daily intraperitoneal injection for six weeks with either HMW-AGEs (20 mg/kg/day) or a control solution. Hemodynamic measurements were performed at sacrifice. Single cardiomyocytes from the left ventricle were obtained by enzymatic dissociation through retrograde perfusion of the aorta. Unloaded cell shortening, time to peak and time to 50% relaxation were measured during field stimulation and normalized to diastolic length. L-type Ca2+ current density (ICaL) and steady-state inactivation of ICaL were measured during whole-cell ruptured patch clamp. Myofilament functional properties were measured in membrane-permeabilized cardiomyocytes. Ultrastructural examination of cardiac tissue was performed using electron microscopy. Results: Rats injected with HMW-AGEs displayed in vivo cardiac dysfunction, characterized by significant changes in left ventricular peak rate pressure rise and decline accompanied with an increased heart mass. Single cardiomyocytes isolated from the left ventricle revealed concentric hypertrophy, indicated by the increase in cellular width. Unloaded fractional cell shortening was significantly reduced in cells derived from the HMW-AGEs group and was associated with slower kinetics. Peak L-type Ca2+ current density was significantly decreased in the HMW-AGEs group. L-type Ca2+ channel availability was significantly shifted towards more negative potentials after HMW-AGEs injection. The impact of HMW-AGEs on myofilament function was measured in membrane-permeabilized cardiomyocytes showing a reduction in passive force, maximal Ca2+ activated force and rate of force development. Ultrastructural examination of cardiac tissue demonstrated adverse structural remodeling in HMW-AGEs group characterized by a disruption of the cyto-architecture, a decreased mitochondrial density and altered mitochondrial function. Conclusion: Our data indicate that HMW-AGEs induce structural and functional cellular remodeling via a different working mechanism as the well-known LMW-AGEs. Results of our research open the door for new strategies targeting HMW-AGEs to improve cardiac outcome