BackgroundRecent studies have shown effective clinical results after arthroscopic Bankart repair (ABR) but have shown several risk factors for re-dislocation after surgery. We evaluated whether patients are at a risk for re-dislocation during the first year after ABR, examined the recurrence rate after ABR, and sought to identify new risk factors.MethodsWe performed ABR using bioabsorbable suture anchors in 102 consecutive shoulders (100 patients) with traumatic anterior shoulder instability. Average patient age and follow-up period was 25.7 (range, 14–40) years and 67.5 (range, 24.5–120) months, respectively. We evaluated re-dislocation after ABR using patient telephone interviews (follow-up rate, 100%) and correlated re-dislocation with several risk factors.ResultsRe-dislocation after ABR occurred in nine shoulders (8.8%), of which seven sustained re-injuries within the first year with the arm elevated at 90° and externally rotated at 90°. Of the remaining 93 shoulders without re-dislocation, 8 had re-injury under the same conditions within the first year. Thus, re-injury within the first year was a risk for re-dislocation after ABR (P < 0.001, chi-squared test). Using multivariate analysis, large Hill-Sachs lesions (odds ratio, 6.77, 95% CI, 1.24–53.6) and <4 suture anchors (odds ratio, 9.86, 95% CI, 2.00–76.4) were significant risk factors for re-dislocation after ABR.ConclusionsThe recurrence rate after ABR is not associated with the time elapsed and that repair strategies should augment the large humeral bone defect and use >3 anchors during ABR.
Successful rotator cuff repair requires biological anchoring of the repaired tendon to the bone. However, the histological structure of the repaired tendon-bone interface differs from that of a normal tendon insertion. We analysed differences between the normal tendon insertion and the repaired tendon-bone interface after surgery in the mechanical properties, histomorphometric analysis, and 3-dimensional ultrastructure of the cells using a rat rotator cuff repair model. Twenty-four adult Sprague-Dawley (SD) rats underwent complete cuff tear and subsequent repair of the supraspinatus tendon. The repaired tendon-bone interface was evaluated at 4, 8, and 12 weeks after surgery. At each time point, shoulders underwent micro-computed tomography scanning and biomechanical testing (N = 6), conventional histology and histomorphometric analysis (N = 6), and ultrastructural analysis with focused ion beam/scanning electron microscope (FIB/SEM) tomography (N = 4). We demonstrated that the cellular distribution between the repaired tendon and bone at 12 weeks after surgery bore similarities to the normal tendon insertion. However, the ultrastructure of the cells at any time point had a different morphology than those of the normal tendon insertion. These morphological differences affect the healing process, partly contributing to re-tearing at the repair site. These results may facilitate future studies of the regeneration of a normal tendon insertion.
The data suggest the relevance of clinical application of HA to accelerate tendon-to-bone healing. It may decrease the number of retears after surgery.
Corticosteroids (CS) or hyaluronic acid (HA) is used in subacromial injection for the conservative treatment of rotator cuff tears (RCT); this study addresses the question of how CS and HA affect the tendon tissue and fibroblasts in vitro and in rats. Cell proliferation assays were performed in human tendon fibroblasts from RCT. Rats underwent surgery to create RCT, and the surgical sites were injected with CS or HA. The rotator cuff tendons were subjected to biomechanical testing, microscopic and immunohistochemical analysis of proliferating cell nuclear antigen (PCNA), and ultrastructural analysis. Cell proliferation was significantly decreased with CS in vitro (p < 0.05). Maximal load of CS-treated tendons was significantly decreased compared with that of HAtreated tendons (p < 0.05), as well as PCNA þ cells at 2 weeks (p < 0.05). Ultrastructural observations of the CS-treated rats detected apoptosis of tendon fibroblasts 24 h after surgery. Histological and biomechanical data 4 weeks after surgery were not significant among the three groups. Unlike HA, CS caused cell death, and inhibition of the proliferation of tendon fibroblasts, leading to a delay of tendon healing involved and a subsequent decrease of biomechanical strength at the surgical site. Keywords: tendon; corticosteroids; hyaluronic acids; totator cuff tears; tendon fibroblast Rotator cuff tears (RCT) occur in the middle-aged and elderly people and cause severe shoulder pain. The prevalence of RCT ranges from 5% to 40% in the general population, 1 increasing linearly with age from the third decade. [2][3][4] In clinical settings, initial treatment of RCT to alleviate shoulder pain and restore shoulder function employs subacromial injection of corticosteroids (CS), administration of nonsteroid antiinflammatory drugs, and physical therapy.
We determined lidocaine's action on torn rotator cuff tendons in vitro and in vivo. For in vitro experiments, cell proliferation and viability assays were performed using tenocytes derived from human torn rotator cuff tendons. For in vivo experiments, acute rotator cuff tears were made on the supraspinatus tendons in the rats' bilateral shoulders; before closure, lidocaine was injected into the shoulder and saline into the contralateral shoulder (control). After sacrifice, the specimens underwent biomechanical testing or histological analysis at 24 h and at 2, 4, and 8 weeks after surgery. The extent of collagen organization and apoptosis were semi-quantitatively evaluated using collagen picrosirius red staining. Apoptosis was examined using TUNEL staining and electron microscopy. Cell proliferation decreased dose-dependently. After exposure to 0.1% lidocaine for 24 h, cell viability decreased. Two and 4 weeks after surgery, the ultimate load to failure decreased more in the lidocaine group than in the control group, with significantly reduced stiffness in the lidocaine group 2 weeks after surgery. Collagen organization significantly decreased in the lidocaine group by 4 weeks after surgery but returned to baseline at 8 weeks. TUNEL staining detected numerous apoptotic tenocytes at the torn tendon edge exposed to lidocaine 24 h after surgery; electron microscopy confirmed the condensed cell nuclei. These changes were not observed in controls. Lidocaine caused cytotoxicity to tenocytes under both conditions, decreased biomechanical properties, and induced apoptosis and delay of collagen organization in this model. Subacromial lidocaine injections in patients with rotator cuff tears should be performed carefully. © 2016 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 34:1620-1627, 2016.
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