36 research outputs found

    The results of using a tendon autograft as a new rotator cable for patients with a massive rotator cuff tear:a technical note and comparative outcome analysis

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    Background: Several surgical reconstructive options are available to treat massive rotator cuff tears (MRCTs). The rotator cable has an important function and we evaluated the clinical result after arthroscopic reconstruction of the rotator cable with an autograft tendon. Methods: A prospective pilot study was performed with inclusion of four patients, average age of 64 years, with an irreparable MRCT. The patients underwent an arthroscopic reconstruction of the rotator cable with the use of the long head of biceps tendon autograft, except for one which was reconstructed with a hamstring tendon. Pre- and postsurgically, the Constant-Murley Score (CMS), Western Ontario Rotator Cuff Index (WORC), Simple Shoulder Test (SST), visual analog scale (VAS) scores, and an MRI was performed. Clinical results of the study group were compared with clinical results of comparable cohort of patients with a MRCT, treated non-operatively with physiotherapy. Results: The CMS score increased after surgery in three of the four patients. The improvement of CMS score was comparable to the improvement of the CMS score encountered in a comparable cohort. The MRI at 12 months follow-up showed that the reconstructed rotator cable was disintegrated in all patients and the rotator cuff was detached and retracted. Conclusions: In our pilot study, arthroscopic reconstruction of the rotator cable using a tendon autograft failed over time and showed no clinical benefit in comparison to the non-operative treatment with physiotherapy. Trial registration: The regional Medical Ethical Committee (Zwolle) gave approval at 14th of October 2016 and assigned no. 16.06100

    Arthroscopic isolated long head of biceps tenotomy in patients with degenerative rotator cuff tears:mid-term clinical results and prognostic factors

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    INTRODUCTION: The long head of biceps tendon is frequently involved in degenerative rotator cuff tears. Therefore, this study explored the clinical results of an isolated biceps tenotomy and identified prognostic factors for improvement in pain and function. MATERIALS AND METHODS: Between 2008 and 2017, an arthroscopic isolated biceps tenotomy was performed on 64 patients with a degenerative rotator cuff tear (> 65 years). Primary outcome was patient-perceived improvement in pain and function. Potential prognostic factors for improvement in pain and function were identified. RESULTS: A perceived improvement in pain was reported in 78% of the patients at three months after surgery and in 75% at a mean follow-up of 4.2 years (1-7 years; n = 55). A perceived improvement in function was observed in 49% of patients at three months and in 76% of patients at follow-up. Patients with a preoperatively normal acromiohumeral distance (> 10 mm) reported an improvement in pain and function significantly more often. Retraction of the supraspinatus tendon Patte 3 was significantly associated with worse functional outcome. CONCLUSIONS: A biceps tenotomy can be a reliable treatment option for patients with symptomatic degenerative cuff tears who fail conservative treatment and have a normal acromiohumeral distance (> 10 mm)

    Psychological symptoms and the MCID of the DASH score in shoulder surgery

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    BACKGROUND: Psychological symptoms are frequently present in patients scheduled for shoulder surgery. The perception of functional disability, activity level and pain in the shoulder is negatively influenced by psychological symptoms, which leads to higher scores of the Disabilities of the Arm, Shoulder and Hand (DASH) questionnaire. The aim of this study was to determine the influence of psychological symptoms on the minimal clinically important difference (MCID) of the DASH score in patients after shoulder surgery. METHODS: In this prospective longitudinal cohort study, 176 patients were included. Group 1 (32 patients) had symptoms of psychological disorders before and after surgery; group 2 had no symptoms of psychological disorders (110 patients). In the remaining patients (34 patients), psychological disorders changed after surgery. Clinical outcome was measured with the change of DASH score and anchor questions for perceived improvement of pain and function after surgery. Symptoms of psychological disorders were identified with the Four-Dimensional Symptom Questionnaire. An anchor-based mean change score technique was used to determine the MCID of the DASH score. RESULTS: DASH scores before and 12 months after shoulder surgery were significantly higher in patients with symptoms of psychological disorders; change of DASH score was not different between the two groups. The MCID of the DASH score was 13.0 [SD 20.7] in the group with symptoms of psychological disorders and 12.7 [SD 17.6] in the group with no symptoms of psychological disorders. We observed no difference (p = 0.559) in the MCID between the group with and the group without symptoms of psychological disorders. CONCLUSION: Symptoms of psychological disorders had a negative effect on the DASH score but no influence on the MCID of the DASH score. The DASH score could be used in future studies to assess the influence of psychological factors on the clinical outcome of treatment

    Accelerated surgery versus standard care in hip fracture (HIP ATTACK): an international, randomised, controlled trial

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    Long-term clinical outcome of arthroscopic Bankart repair with suture anchors

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    Background: The most common surgical technique in traumatic anterior shoulder instability is the arthroscopic Bankart repair, which has excellent short-term results. The long-term results of the arthroscopic Bankart repair are less frequently studied, with a high recurrence rate of 23% to 35%. The aim of this study was to evaluate the medium-term to long-term results of arthroscopic Bankart repair using suture anchors and to identify specific risk factors for recurrent instability. Methods: Included were 147 patients after traumatic anterior shoulder dislocation who underwent an arthroscopic Bankart repair. The primary outcome was recurrent instability, defined as dislocation or subluxation as perceived by the patients. The secondary outcome was subjective shoulder stability and function as well as quality of life, evaluated using the Western Ontario Shoulder Instability Index, the Simple Shoulder Test, and the 12-Item Short Form Health Survey. Prognostic factors for recurrent instability were analyzed. Results: Recurrent instability occurred in 22% of patients with a mean follow-up of 6.3 years. Survival at 5 and 10 years without recurrent instability was 79% and 78%, respectively (95% confidence interval, 72%-85% and 71%-85%, respectively). The Western Ontario Shoulder Instability Index score, the Simple Shoulder Test score, and the 12-item Short Form Physical Component Summary improved significantly in the nonrecurrence group (P <.001, P = .004, and P = .002, respectively). Younger age and use of fewer than 3 anchors were associated with a higher risk of recurrent dislocation (P = .008 and P = .039, respectively). Conclusion: We found an overall recurrent instability rate of 22% (dislocation or subluxation). Good long-term results were observed after arthroscopic Bankart repair in patients older than 20 years with 3 or more suture anchors used. (C) 2018 Journal of Shoulder and Elbow Surgery Board of Trustees. All rights reserved

    Sotos Syndrome Is Associated with Deregulation of the MAPK/ERK-Signaling Pathway

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    <div><p>Sotos syndrome (SoS) is characterized by tall stature, characteristic craniofacial features and mental retardation. It is caused by haploinsufficiency of the <em>NSD1</em> gene. In this study, our objective was to identify downstream effectors of NSD1 and to map these effectors in signaling pathways associated with growth. Genome-wide expression studies were performed on dermal fibroblasts from SoS patients with a confirmed <em>NSD1</em> abnormality. To substantiate those results, phosphorylation, siRNA and transfection experiments were performed. A significant association was demonstrated with the Mitogen-Activated Protein Kinase (MAPK) pathway. Members of the fibroblast growth factor family such as <em>FGF4</em> and <em>FGF13</em> contributed strongly to the differential expression in this pathway. In addition, a diminished activity state of the MAPK/ERK pathway was demonstrated in SoS. The Ras Interacting Protein 1 (RASIP1) was identified to exhibit upregulated expression in SoS. It was shown that RASIP1 dose-dependently potentiated bFGF induced expression of the MAPK responsive SBE reporter providing further support for a link between NSD1 and the MAPK/ERK signaling pathway. Additionally, we demonstrated <em>NSD1</em> expression in the terminally differentiated hypertrophic chondrocytes of normal human epiphyseal growth plates. In short stature syndromes such as hypochondroplasia and Noonan syndrome, the activation level of the FGF-MAPK/ERK-pathway in epiphyseal growth plates is a determining factor for statural growth. In analogy, we propose that deregulation of the MAPK/ERK pathway in SoS results in altered hypertrophic differentiation of <em>NSD1</em> expressing chondrocytes and may be a determining factor in statural overgrowth and accelerated skeletal maturation in SoS.</p> </div

    Hypoxia inhibits hypertrophic differentiation and endochondral ossification in explanted tibiae.

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    Hypertrophic differentiation of growth plate chondrocytes induces angiogenesis which alleviates hypoxia normally present in cartilage. In the current study, we aim to determine whether alleviation of hypoxia is merely a downstream effect of hypertrophic differentiation as previously described or whether alleviation of hypoxia and consequent changes in oxygen tension mediated signaling events also plays an active role in regulating the hypertrophic differentiation process itself.Fetal mouse tibiae (E17.5) explants were cultured up to 21 days under normoxic or hypoxic conditions (21% and 2.5% oxygen respectively). Tibiae were analyzed on growth kinetics, histology, gene expression and protein secretion.The oxygen level had a strong influence on the development of explanted fetal tibiae. Compared to hypoxia, normoxia increased the length of the tibiae, length of the hypertrophic zone, calcification of the cartilage and mRNA levels of hypertrophic differentiation-related genes e.g. MMP9, MMP13, RUNX2, COL10A1 and ALPL. Compared to normoxia, hypoxia increased the size of the cartilaginous epiphysis, length of the resting zone, calcification of the bone and mRNA levels of hyaline cartilage-related genes e.g. ACAN, COL2A1 and SOX9. Additionally, hypoxia enhanced the mRNA and protein expression of the secreted articular cartilage markers GREM1, FRZB and DKK1, which are able to inhibit hypertrophic differentiation.Collectively our data suggests that oxygen levels play an active role in the regulation of hypertrophic differentiation of hyaline chondrocytes. Normoxia stimulates hypertrophic differentiation evidenced by the expression of hypertrophic differentiation related genes. In contrast, hypoxia suppresses hypertrophic differentiation of chondrocytes, which might be at least partially explained by the induction of GREM1, FRZB and DKK1 expression

    Geneplots of the probe sets influencing the MAPK pathway.

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    <p>Geneplots are shown for the 50 most influential probe sets from the KEGG MAPK pathway (A) and for the GO-term MAPKKK cascade (B) after stimulation with RA that contribute to the differential pathway expression in SoS and control. Probe sets are scaled to unit standard deviations and the height of the bars are the number of standard deviations above the cut-off level of 0.7. Higher bars indicate higher influence on the pathway. Probe sets with the highest influence on the pathway (i.e. FGF13 in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0049229#pone-0049229-g001" target="_blank">Figure 1A</a> and TNIK in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0049229#pone-0049229-g001" target="_blank">Figure 1B</a>) are depicted on the left. Corresponding gene names are written below each bar.</p
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