Distal junctional kyphosis in patients with Scheuermann’s disease: a retrospective radiographic analysis

Purpose To investigate the relationship between preoperative and postoperative spinopelvic alignment and occurrence of DJK/DJF. Study design/setting This was a retrospective observational cohort study. Patient sample The sample included 40 patients who underwent posterior correction of SK from January 2006 to December 2014. Outcome measures Correlation analysis between the preoperative and postoperative spinopelvic alignment parameters and development of DJK over the course of the study period were studied. Methods Whole spine X-rays obtained before surgery, 3 months after surgery and at the latest follow-up were analyzed. The following parameters were measured: maximum of thoracic kyphosis (TK), lumbar lordosis (LL), sagittal vertical axis (SVA), pelvic incidence (PI), pelvic tilt (PT), sacral slope (SS), lower instrumented vertebra (LIV) and LIV plumb line. Development of DJK was considered as the primary end point of the study. The patient population was split into a control and DJK group, with 34 patients and 6 patients, respectively. Statistic analysis was performed using unpaired t test for normal contribution and Mann–Whitney test for skew distributed values. The significance level was set to 0.05. Results DJK occurred in 15% (n = 6) over the study period. There was a significantly lower postoperative TK for the group with DJK (42.4 ± 5.3 vs 49.8 ± 6.7, p = 0.015). LIV plumb line showed higher negative values in the DJK group (−43.6 ± 25.1 vs −2.2 ± 17.8, p = 0.0435). Furthermore, postoperative LL changes were lower for the DJK group (33.84 ± 13.86% vs 31.77 ± 14.05, p < 0.0001.) The age of the patients who developed DJK was also significantly lower than that of the control group (16.8 ± 1.7 vs 19.6 ± 4.9, p = 0.0024.) Conclusions SK patients who developed DJK appeared to have a significantly higher degree of TK correction and more negative LIV plumb line. In addition, there may be a higher risk for DJK in patients undergoing corrective surgery at a younger age

Spontaneous DNA damage to the nuclear genome promotes senescence,redox imbalance and aging

Accumulation of senescent cells over time contributes to aging and age-related diseases. However, what drives senescence in vivo is not clear. Here we used a genetic approach to determine if spontaneous nuclear DNA damage is sufficient to initiate senescence in mammals. Ercc1-/Δ mice with reduced expression of ERCC1-XPF endonuclease have impaired capacity to repair the nuclear genome. Ercc1-/Δ mice accumulated spontaneous, oxidative DNA damage more rapidly than wild-type (WT) mice. As a consequence, senescent cells accumulated more rapidly in Ercc1-/Δ mice compared to repair-competent animals. However, the levels of DNA damage and senescent cells in Ercc1-/Δ mice never exceeded that observed in old WT mice. Surprisingly, levels of reactive oxygen species (ROS) were increased in tissues of Ercc1-/Δ mice to an extent identical to naturally-aged WT mice. Increased enzymatic production of ROS and decreased antioxidants contributed to the elevation in oxidative stress in both Ercc1-/Δ and aged WT mice. Chronic treatment of Ercc1-/Δ mice with the mitochondrial-targeted radical scavenger XJB-5–131 attenuated oxidative DNA damage, senescence and age-related pathology. Our findings indicate that nuclear genotoxic stress arises, at least in part, due to mitochondrial-derived ROS, and this spontaneous DNA damage is sufficient to drive increased levels of ROS, cellular senescence, and the consequent age-related physiological decline

Spontaneous DNA damage to the nuclear genome promotes senescence, T redox imbalance and aging

Accumulation of senescent cells over time contributes to aging and age-related diseases. However, what drives senescence in vivo is not clear. Here we used a genetic approach to determine if spontaneous nuclear DNA damage is sufficient to initiate senescence in mammals. Ercc1-/Δ mice with reduced expression of ERCC1-XPF endonuclease have impaired capacity to repair the nuclear genome. Ercc1-/Δ mice accumulated spontaneous, oxidative DNA damage more rapidly than wild-type (WT) mice. As a consequence, senescent cells accumulated more rapidly in Ercc1-/Δ mice compared to repair-competent animals. However, the levels of DNA damage and senescent cells in Ercc1-/Δ mice never exceeded that observed in old WT mice. Surprisingly, levels of reactive oxygen species (ROS) were increased in tissues of Ercc1-/Δ mice to an extent identical to naturally-aged WT mice. Increased enzymatic production of ROS and decreased antioxidants contributed to the elevation in oxidative stress in both Ercc1-/Δ and aged WT mice. Chronic treatment of Ercc1-/Δ mice with the mitochondrial-targeted radical scavenger XJB-5–131 attenuated oxidative DNA damage, senescence and age-related pathology. Our findings indicate that nuclear genotoxic stress arises, at least in part, due to mitochondrial-derived ROS, and this spontaneous DNA damage is sufficient to drive increased levels of ROS, cellular senescence, and the consequent age-related physiological decline

Correction of complex lower limb angular deformities with or without length discrepancy in children using the TL-HEX hexapod system: comparison of clinical and radiographical results

The aim of this study was to compare clinical and radiographical results for treatment of lower limb multiaxial deformities +/- limb length discrepancy (LLD) of at least 2 cm with the Truelok hexapod fixator system (TL-HEX). All consecutive cases of lower limb multiaxial deformities were included. Patients were divided in two groups: group 1, lower limb angular deformity+LLD less than 2 cm, and group 2, lower limb angular deformity+LLD of at least 2 cm. Only patients with age younger than or equal to 20 years and follow-up of 6 months after removal of the external fixator were included. A total of 27 (six femur and 39 tibia treated) and 20 patients (12 femur and 19 tibia) were enrolled in groups 1 and 2, respectively. Complete correction of the deformity was achieved in 90 and 96% of the patients in groups 1 and 2, respectively. There were no differences in terms of external fixator, maturation, and distraction indexes between the two groups and between different anatomical sites. Good to excellent functional results (ASAMI score) were obtained in 93% of patients in group 1 and 75% in group 2 (P=0.01). Complication rate was similar between the two groups (7.4 vs. 10%, respectively). Average follow-up after removal of the external fixator was 25.6 (range: 7.0-54.0) months. The TL-HEX external fixator system allows a predictable correction of complex lower limb deformities regardless of the presence of LLD. Although complication rate is similar between the two groups, lower functional outcomes can be expected in patients with significant preoperative LLD

Safety and efficacy of anterior vertebral body tethering in the treatment of idiopathic scoliosis

AimsSpinal fusion remains the gold standard in the treatment of idiopathic scoliosis. However, anterior vertebral body tethering (AVBT) is gaining widespread interest, despite the limited data on its efficacy. The aim of our study was to determine the clinical efficacy of AVBT in skeletally immature patients with idiopathic scoliosis.MethodsAll consecutive skeletally immature patients with idiopathic scoliosis treated with AVBT enrolled in a longitudinal, multicentre, prospective database between 2013 and 2016 were analyzed. All patients were treated by one of two surgeons working at two independent centres. Data were collected prospectively in a multicentre database and supplemented retrospectively where necessary. Patients with a minimum follow-up of two years were included in the analysis. Clinical success was set a priori as a major corona) Cobb angle of &lt; 35 degrees at the most recent follow-up.ResultsA total of 57 patients were included in the study. Their mean age was 12.7 years (SD 1.5; 8.2 to 16.7), with 95% being female. The mean preoperative Sanders score and Risser grade was 3.3 (SD 1.2), and 0.05 (0 to 3), respectively. The majority were thoracic tethers (96.5%) and the mean follow-up was 40.4 months (SD 9.3). The mean preoperative major curve of 51 degrees (SD 10.9 degrees; 31 degrees to 81 degrees) was significantly improved to a mean of 24.6 degrees (SD 11.8 degrees; 0 degrees to 57 degrees) at the first postoperative visit (45.6% (SD 17.6%; 7% to 107%); p &lt; 0.001)) with further significant correction to a mean of 16.3 degrees (SD 12.8 degrees; -12 to 55; p &lt; 0.001) at one year and a significant correction to a mean of 23 degrees (SD 15.4 degrees; -18 degrees to 57 degrees) at the final follow-up (42.9% (-16% to 147%); p &lt; 0.001). Clinical success was achieved in 44 patients (77%). Most patients reached skeletal maturity, with a mean Risser score of 4.3 (SD 1.02), at final follow-up. The complication rate was 28.1% with a 15.8% rate of unplanned revision procedures.ConclusionAVBT is associated with satisfactory correction of deformity and an acceptable complication rate when used in skeletally immature patients with idiopathic scoliosis. Improved patient selection and better implant technology may improve the 15.8% rate of revision surgery in these patients. Further scrutiny of the true effectiveness and long-term risks of this technique remains critical

Onset of a Charcot spinal arthropathy at a level lacking surgical arthrodesis in a paraplegic patient with traumatic cord injury

The study design included a case report of Charcot spinal arthropathy treated with posterior and anterior spinal instrumentation. The objective of the study was to report an unusual case of Charcot spinal arthropathy as a late complication of traumatic spinal cord injury in a patient previously treated with a long posterior thoraco-lumbar instrumentation and postero-lateral fusion. A 33-year-old man with T10–T11 complete paraplegia presented with focal low back pain, kyphotic deformity of the lumbar region with L2–L3 fracture–dislocation and hardware failure. Our treatment consisted of a circumferential arthrodesis performed with a combined anterior and posterior approach. Spinal stabilization was achieved and the patient was pain free and able to resume a sitting posture. This report suggests that the development of a Charcot spine arthropathy must always be considered as a late complication of a spinal cord injury. Moreover, we would emphasize the fundamental role of a strict clinical and radiological follow-up in order to detect an early Charcot spine complication

Investigating the role of DNA damage in tobacco smoking-induced spine degeneration

Tobacco smoking is a key risk factor for spine degeneration. However, the underlying mechanism by which smoking induces degeneration is not known. Recent studies implicate DNA damage as a cause of spine and intervertebral disc degeneration. Because tobacco smoke contains many genotoxins, we hypothesized that tobacco smoking promotes spine degeneration by inducing cellular DNA damage

NF-κB inhibition delays DNA damage–induced senescence and aging in mice

The accumulation of cellular damage, including DNA damage, is thought to contribute to aging-related degenerative changes, but how damage drives aging is unknown. XFE progeroid syndrome is a disease of accelerated aging caused by a defect in DNA repair. NF-κB, a transcription factor activated by cellular damage and stress, has increased activity with aging and aging-related chronic diseases. To determine whether NF-κB drives aging in response to the accumulation of spontaneous, endogenous DNA damage, we measured the activation of NF-κB in WT and progeroid model mice. As both WT and progeroid mice aged, NF-κB was activated stochastically in a variety of cell types. Genetic depletion of one allele of the p65 subunit of NF-κB or treatment with a pharmacological inhibitor of the NF-κB–activating kinase, IKK, delayed the age-related symptoms and pathologies of progeroid mice. Additionally, inhibition of NF-κB reduced oxidative DNA damage and stress and delayed cellular senescence. These results indicate that the mechanism by which DNA damage drives aging is due in part to NF-κB activation. IKK/NF-κB inhibitors are sufficient to attenuate this damage and could provide clinical benefit for degenerative changes associated with accelerated aging disorders and normal aging