Long-term results after thoracoscopic anterior spondylodesis with or without posterior stabilization of unstable incomplete burst fractures of the thoracolumbar junction: a prospective cohort study.

BACKGROUND: Minimally invasive, thoracoscopic anterior spondylodesis (MIAS) is an established treatment for burst fractures of the thoracolumbar spine. Good restoration of the local sagittal alignment and good functional results have been reported. The aim of this study was to evaluate long-term results of MIAS in patients with incomplete burst fractures and to analyze the influence on global sagittal alignment, clinical outcomes, and adjacent segment degeneration. METHODS: From 2002 to 2003, 18 patients were treated with MIAS for incomplete thoracolumbar burst fractures. Mono-segmental spondylodesis was performed with an iliac crest bone graft and bisegmental spondylodesis with a titanium cage. In this single-center prospective cohort study, 15 patients were available for follow-up (FU) after an average of 12.9 years (12.1-14.4). Seven patients were treated with a combined anterior and posterior instrumentation and eight patients with anterior spondylodesis only. The primary clinical outcome parameter was the Oswestry Disability Index (ODI); secondary parameters were the Short Form 36 (SF36) and the visual analog scale (VAS spine). Full spine radiographs were assessed for bisegmental Cobb angle, alignment parameters, and signs of adjacent segment degeneration (ASD). RESULTS: ODI evaluation showed a mean impairment of 11.7% with minimal limitations in 13 patients. Neither a significant deterioration over time nor significant differences between both therapy strategies were found in the clinical scores at the latest follow-up. The mean bisegmental increase of regional malalignment of reduction was 8.8° (± 7.3°) with no significant correlation to any clinical outcome scores. The majority of patients had no signs of adjacent segment degeneration. Two patients showed minor radiologic changes. All patients had a balanced sagittal spine profile. CONCLUSIONS: In conclusion, MIAS leads to good clinical results with-in majority-minimal spine-related impairment at the latest follow-up. No significant deterioration at 12-year FU was detectable compared to the 6-year results for the SF36 and VAS spine scores. There was no association between sagittal alignment, clinical outcome scores, and ASD. TRIAL REGISTRATION: The study was retrospectively registered in the German Clinical Trials Register ( Nr.00015656 ).

Primary single suture anchor re-fixation of anterior cruciate ligament proximal avulsion tears leads to good functional mid-term results: a preliminary study in 12 patients.

BACKGROUND: Current studies demonstrate encouraging short-term results after primary anterior cruciate ligament (ACL) suture anchor repair. However, earlier studies reported deterioration of knee function at 5-year follow-up following good clinical short-term recovery. Therefore, the aim of this study was to evaluate clinical long-term results after primary ACL repair at a minimum 5-year follow-up. METHODS: In a retrospective study, 13 patients were included between 2009 and 2012. Inclusion criteria were an acute proximal, femoral avulsion tear of the ACL with good tissue quality and sagittal instability in a healthy, demanding patient. Patients suffering proximal tibial fractures, arthrosis, or multiligamentous injuries of the knee were excluded. The ACL was anchored to the footprint by a single 2.9-mm push lock anchor, followed by additional microfracturing. For follow-up, patients were evaluated according to Lysholm score, modified Cincinnati score, and Tegner activity score. Clinical examination was performed using Lachman and pivot-shift testing and range of motion and sagittal stability measurement, using a Rolimeter. RESULTS: Mean follow-up was 79 (range 60 to 98) months. One patient was lost to follow-up, and 11 out of 12 patients were examined clinically. Eight patients achieved good subjective and clinical outcome. One patient suffered an early re-tear, and one patient with additional patellar tendon tear and one patient with polyarthritis demonstrated poor subjective and clinical results due to lasting instability. Seven out of 12 patients reached preoperative Tegner activity score postoperatively again. The mean Lysholm score was 85.3 points, mean subjective IKDC score was 87.3 points, and mean modified Cincinnati score was 83.8 points. Rolimeter measurements demonstrated a mean side-to-side difference of 2 (range 1-5) mm. CONCLUSION: In the current study, primary surgical re-fixation of proximal, femoral ACL avulsion tears using single suture anchor repair resulted in good to excellent clinical mid-term outcomes. However, in cases of additional serious damage to extensor structures or systemic rheumatic disease, loss of function and unsatisfying clinical results occurred. Further prospective randomized controlled trials are necessary to confirm the encouraging long-term results of this study. TRIAL REGISTRATION: Bavarian National Medical Chamber of Physicians, file number 2016-095. German Clinical Trials ( DRKS00013059 ).

Platelet GPVI binds to collagenous structures in the core region of human atheromatous plaque and is critical for atheroprogression in vivo.

Platelet adhesion to the atherosclerotic vascular wall induces thrombosis and boosters vascular inflammation and atheroprogression. In the present study we studied the binding of the platelet collagen receptor glycoprotein (GP) VI to human atherosclerotic plaques (AP) and the role of GPVI-mediated platelet adhesion for atheroprogression. Soluble GPVI-Fc fusion protein bound to immobilized collagen type I, collagen type III, and predominantly to the core region of human carotid atheromatous plaques. The pattern of GPVI-Fc binding was similar to the immunostaining pattern of collagen type III and differed from the immunostaining of collagen type I, which was more intense in the cap than in the core. Plaque-induced platelet aggregation in stirred blood and platelet adhesion/aggregate formation under flow were inhibited by the anti-GPVI monoclonal antibody 5C4 or by pretreatment of plaques with anti-collagen type I and anti-collagen type III antibody, or GPVI-Fc. However, there was no correlation between GPVI-Fc binding and platelet aggregating activity of individual plaques. GPVI bound also to atherosclerotic arteries of ApoE-deficient mice in vivo as assessed by small animal positron emission tomography (PET). Prolonged administration of soluble GPVI attenuated atheroprogression in ApoE-deficient mice. In humans, GPVI binding to collagenous type I and type III structures of the plaque core region mediates plaque-induced platelet adhesion and aggregation, but GPVI binding is not the sole platelet-activating determinant of plaques. In mice, GPVI-mediated platelet adhesion to the atherosclerotic vascular wall is involved in atheroprogression in vivo. Taken together, our data suggests that GPVI is a relevant target to prevent atherothrombotic events and atheroprogression.