Double-pulley, V-shaped fixation technique for arthroscopic repair of ideberg type IA glenoid fracture.

Different techniques have been described for glenoid fractures, there is still a need for safe and effective agents to promote outcomes. From January 2016 to April 2021, the clinical data of 17 patients with pulley type IA fractures treated by the V-shaped fixation technique under shoulder arthroscopy were retrospectively analyzed. Preoperative X-ray, CT, and MRI examinations were completed. The functional score of the shoulder joint, such as the visual analog scale (VAS), Constant score, and Modified Rowe score, was used to evaluate the preoperative and final follow-up clinical outcomes. The active shoulder range of motion (ROM) was also collected preoperatively and at the final postoperative follow-up. Accordingly, intraoperative and postoperative complications were also observed. The mean follow-up was 49.52 months (16-79 months). The patients' follow-up exams showed that shoulder joint flexion, abduction, external rotation, internal rotation, and pain were not significantly different from those of the contralateral side (p > .05). The mean Constant score was 83.52 (58-98), and the average Modified Rowe score was 94.29 (70-100). X-ray and CT films of all cases showed good healing without articular depression or steps. Three patients had traumatic arthritis, with VAS <3 pain. No postoperative complications, such as infections, nerve or vessel damage, or suture anchor problems occurred during the follow-up period. Using the Double-pull, V-shaped fixation technique can stabilize the reduction of glenoid fractures while reducing the possibility of bone destruction. It is a good solution and provides an opportunity to treat rotator cuff tears associated with the procedure.

The femoral anterior tangent line could serve as a reliable alternative reference axis for distal femoral rotational alignment in total knee arthroplasty: an MRI-based study.

Background: This study aimed to evaluate the reference value of the femoral anterior tangent (FAT) line as a guidance of distal femoral rotation on magnetic resonance images (MRI). Methods: We retrospectively included 81 patients (106 knees) diagnosed as ailing from primary knee osteoarthritis. The indirect rotational axes including the FAT line, the perpendicular line to the anteroposterior axis (pAPA), and the posterior condylar axis (PCA) were identified on MRI, and their angles related to the clinical transepicondylar axis (cTEA) or surgical transepicondylar axis (sTEA) were measured. The patients were further divided into subgroups according to the Kellgren-Lawrence (K-L) grades, the joint-line convergence angle (JLCA), and the arithmetic hip-knee-ankle angle (aHKA) to assess the variance of different rotational reference axes. Results: The FAT line was -11.8° ± 3.6° internally rotated to the cTEA and -7.5° ± 3.6° internally rotated to the sTEA. The FAT/cTEA angle and the FAT/sTEA angle shared a similar frequency distribution pattern but a little greater variance to the pAPA/cTEA angle and the PCA/cTEA angle. The PCA/cTEA angle in the JLCA |x| ≥ 6° subgroup was significantly smaller than in the two other JLCA subgroups. The pAPA/cTEA angle and the PCA/cTEA angle also presented statistical significance within the aHKA subgroups. While the FAT/cTEA angle and the FAT/sTEA angle demonstrated superior stability among the different K-L grades, JLCA subgroups, and aHKA subgroups. Conclusion: The FAT line was less affected by the degree of knee osteoarthritis and lower limb alignment, which could serve as a reliable alternative reference axis for the distal femoral rotational alignment in total knee arthroplasty.

Investigation of salmon calcitonin in regulating fibrosis-related molecule production and cell-substrate adhesion in frozen shoulder synovial/capsular fibroblasts.

The purpose of this study was to evaluate the effect of salmon calcitonin (sCT) on improving fibrosis-related indicators in frozen shoulder synovial/capsular fibroblasts (SCFs) and detect the potential downstream pathway. Quantitative real-time polymerase chain reaction and cell-substrate adhesion assays were used to measure alterations in fibrosis-related molecule expression and the cell adhesion ability of frozen shoulder SCFs after treatment with range concentrations of sCT. The presence of calcitonin receptors (CTRs) in shoulder joint synovial/capsular tissue samples was detected by immunohistochemistry (IHC). The downstream pathways of sCT in SCFs were further explored by utilizing three classical pathway inhibitors. With the addition of sCT to the culture medium of frozen shoulder SCFs, the messenger RNA (mRNA) expression of collagen type I (COL1A1), COL3A1, fibronectin 1, laminin 1, transforming growth factor-ß1 (TGF-ß1), and interleukin-1α (IL-1α) showed a descending trend as the sCT concentration increased. Treatment with sCT increased the expression of vascular endothelial growth factor and IL-6 in a dose-dependent manner. The enhanced adhesion ability of frozen shoulder SCFs gradually diminished with increasing concentrations of sCT. By using IHC, the CTR was detected extensively in the frozen shoulder joint synovium and capsule. Blocking the protein kinase C (PKC) pathway reversed the sCT-mediated suppression of COL1A1 production. Blocking the PKC or protein kinase A (PKA) pathway eliminated the sCT-induced inhibition of TGF-ß1 production. This study demonstrated that sCT effectively improved the mRNA expression of fibrosis-related molecules and decreased the enhanced cell-substrate adhesion ability of frozen shoulder SCFs. sCT might achieve these effects by interacting with the CTR that is expressed on the SCF surface and by activating the downstream PKC or PKA pathway.

The Effectiveness and Safety of Utilizing Mobile Phone-Based Programs for Rehabilitation After Lumbar Spinal Surgery: Multicenter, Prospective Randomized Controlled Trial.

BACKGROUND: Rehabilitation is crucial for postoperative patients with low back pain (LBP). However, the implementation of traditional clinic-based programs is limited in developing countries, such as China, because of the maldistribution of medical resources. Mobile phone-based programs may be a potential substitute for those who have no access to traditional rehabilitation. OBJECTIVE: The aim of this study was to examine the efficacy of mobile phone-based rehabilitation systems in patients who underwent lumbar spinal surgery. METHODS: Patients who accepted spinal surgeries were recruited and randomized into 2 groups of rehabilitation treatments: (1) a mobile phone-based eHealth (electronic health) program (EH) or (2) usual care treatment (UC). The primary outcomes were (1) function and pain status assessed by the Oswestry Disability Index (ODI) and (2) the visual analog scale (VAS). Secondary outcomes were (1) general mental health and (2) quality of life (Likert scales, EuroQol-5 Dimension health questionnaire, and 36-item Short-Form Health Survey). All the patients were assessed preoperatively and then at 3, 6, 12, and 24 months postoperatively. RESULTS: A total of 168 of the 863 eligible patients were included and randomized in this study. Our analysis showed that the improvement of primary outcomes in the EH group was superior to the UC group at 24 months postoperatively (ODI mean 7.02, SD 3.10, P<.05; VAS mean 7.59, SD 3.42, P<.05). No significant difference of primary outcomes was found at other time points. A subgroup analysis showed that the improvements of the primary outcomes were more significant in those who completed 6 or more training sessions each week throughout the trial (the highest compliance group) compared with the UC group at 6 months (ODI mean 17.94, SD 5.24, P<.05; VAS mean 19.56, SD 5.27, P<.05), 12 months (ODI mean 13.39, SD 5.32, P<.05; VAS mean 14.35, SD 5.23, P<.05), and 24 months (ODI mean 18.80, SD 5.22, P<.05; VAS mean 21.56, SD 5.28, P<.05). CONCLUSIONS: This research demonstrated that a mobile phone-based telerehabilitation system is effective in self-managed rehabilitation for postoperative patients with LBP. The effectiveness of eHealth was more evident in participants with higher compliance. Future research should focus on improving patients' compliance. TRIAL REGISTRATION: Chinese Clinical Trial Registry ChiCTR-TRC-13003314; http://www.chictr.org.cn/showproj.aspx?proj=6245 (Archived by WebCite at http://www.webcitation.org/766RAIDNc).

Comparison of Knee Stability and Synovial Fluid Alterations in Anterior Cruciate Ligament Reconstruction With a Hamstring Autograft or an Allograft.

This study compared knee stability and alterations in the composition of synovial fluid among patients who underwent arthroscopic anterior cruciate ligament (ACL) reconstruction with either a hamstring autograft or a hamstring allograft. This prospective cohort study enrolled 175 patients. Of these patients, 90 underwent hamstring tendon autograft ACL reconstruction. The remaining patients (n=85) underwent hamstring tendon allograft ACL reconstruction. All of the patients had a minimum of 1 year of follow-up (mean, 2.5 years). Side-to-side differences and the proportion of mononuclear cells in knee joint synovial fluid were measured at 5 time points (preoperatively and at postoperative weeks 1, 3, 6, and 12). During the early postoperative phase, side-to-side knee laxity was greater among the allograft group compared with the autograft group (P<.001). Additionally, among the allograft group, the proportion of mononuclear cells remained high at weeks 6 and 12 (mean, 90.0% and 88.9%, respectively) compared with a normal level in the autograft group (mean, 45.1% and 65.7%, separately). However, no significant difference was found between the 2 groups at final follow-up for range of motion, results of the Lachman test, results of the anterior drawer test, results of the pivot shift test, Lysholm score, bone tunnel enlargement, and graft failure rate (P>.05). These findings showed that, in the early postoperative phase, ACL reconstruction with a hamstring allograft resulted in greater knee laxity and immunologic response compared with the hamstring autograft group. However, at relatively long-term follow-up, both grafts achieved similar objective and subjective outcomes. [Orthopedics. 2017; 40(5):e892-e897.].

Whole-Genome Expression Analysis and Signal Pathway Screening of Synovium-Derived Mesenchymal Stromal Cells in Rheumatoid Arthritis.

Synovium-derived mesenchymal stromal cells (SMSCs) may play an important role in the pathogenesis of rheumatoid arthritis (RA) and show promise for therapeutic applications in RA. In this study, a whole-genome microarray analysis was used to detect differential gene expression in SMSCs from RA patients and healthy donors (HDs). Our results showed that there were 4828 differentially expressed genes in the RA group compared to the HD group; 3117 genes were upregulated, and 1711 genes were downregulated. A Gene Ontology analysis showed significantly enriched terms of differentially expressed genes in the biological process, cellular component, and molecular function domains. A Kyoto Encyclopedia of Genes and Genomes analysis showed that the MAPK signaling and rheumatoid arthritis pathways were upregulated and that the p53 signaling pathway was downregulated in RA SMSCs. Quantitative real-time polymerase chain reaction was applied to verify the expression variations of the partial genes mentioned above, and a western blot analysis was used to determine the expression levels of p53, p-JNK, p-ERK, and p-p38. Our study found that differentially expressed genes in the MAPK signaling, rheumatoid arthritis, and p53 signaling pathways may help to explain the pathogenic mechanism of RA and lead to therapeutic RA SMSC applications.

[COMPARISON OF TUMOR NECROSIS FACTOR α INDUCED APOPTOSIS BETWEEN SYNOVIUM-DERIVED MESENCHYMAL STEM CELLS AND BONE MARROW MESENCHYMAL STEM CELLS].

OBJECTIVE: To investigate the anti-apoptotic ability of synovium-derived mesenchymal stem cells (SMSCs) by comparing the apoptosis induced by tumor necrosis factor α (TNF-α) between SMSCs and bone marrow mesenchymal stem cells (BMSCs). METHODS: SMSCs and BMSCs were isolated with tissue adhering and density gradient centrifugation respectively, and cells at passages 3-5 were used in further experiments. After immunophenotype identification and differentiation induction, cells were divided into 4 groups. In the experimental groups, apoptosis of SMSCs and BMSCs were induced by 20 ng/mL TNF-α and 10 µg/mL cycloheximide, and cells were cultured in normal culture medium in the control groups. Cellular morphology were observed by inverted phase contrast microscope. After apoptosis induction for 24 hours, cell viability was determined by cell counting kit 8 assay and apoptotic index was detected by flow cytometer. Moreover, the level of Cleaved Caspase-8, 3 were determined by Western blot. RESULTS: Both SMSCs and BMSCs accorded with the definition criteria of MSCs according to results of immunophenotype identification and differentiation induction. After apoptosis induction, cells became shrinking and partially floated and cellular morphologies became worse than those in the control groups. After apoptosis induction for 24 hours, cell viabilities of SMSCs and BMSCs in the control groups were both 100%, and no apoptotic cells were observed. However, cell viabilities of SMSCs and BMSCs in the experimental groups were 60.13% ± 8.63% and 46.55% ± 10.54% respectively, which were both significantly lower than those in the control groups (P < 0.05), and cell viability in the SMSCs experimental group was significantly higher than that in the BMSCs experimental group (t = 3.152, P = 0.006). The apoptotic index was 36.54% ± 8.63% in the SMSCs experimental group and was 53.77% ± 11.52% in the BMSCs experimental group, both were significantly higher than the control groups (1.12% ± 0.24% and 1.35% ± 0.31%) (P < 0.05). What's more, it was significantly lower in SMSCs experimental group than that in BMSCs experimental group (t = 3.785, P = 0.001). Moreover, no expression of Cleaved Caspase-8, 3 was detected in the control groups. But the levels of Cleaved Caspase-8, 3 were significantly enhanced in the experimental groups and they were lower in SMSCs than in BMSCs (t = 13.870, P = 0.000; t = 7.309, P = 0.000). CONCLUSION: TNF-α induced apoptosis is lower in SMSCs than in BMSCs, which means that SMSCs may have stronger anti-apoptosis ability than BMSCs.

Autophagy Plays a Protective Role in Tumor Necrosis Factor-α-Induced Apoptosis of Bone Marrow-Derived Mesenchymal Stem Cells.

Bone marrow-derived mesenchymal stem cells (BMSCs) are being broadly investigated for treating numerous inflammatory diseases. However, the low survival rate of BMSCs during the transplantation process has limited their application. Autophagy can maintain cellular homeostasis and protect cells against environmental stresses. Tumor necrosis factor-α (TNF-α) is an important inflammatory cytokine that can induce both autophagy and apoptosis of BMSCs. However, the actual role of autophagy in TNF-α-induced apoptosis of BMSCs remains poorly understood. In the current study, BMSCs were treated with TNF-α/cycloheximide (CHX), and cell death was examined by the Cell Counting Kit-8, Hoechst 33342 staining, and flow cytometric analysis as well as by the level of caspase-3 and caspase-8. Meanwhile, autophagic flux was examined by analyzing the level of microtubule-associated protein light chain 3 B (LC3B)-II and SQSTEM1/p62 and by examining the amount of green fluorescent protein-LC3B by fluorescence microscopy. Then, the cell death and autophagic flux of BMSCs were examined after pretreatment and cotreatment with 3-methyladenine (3-MA, autophagy inhibitor) or rapamycin (Rap, autophagy activator) together with TNF-α/CHX. Moreover, BMSCs pretreated with lentiviruses encoding short hairpin RNA of beclin-1 (BECN1) were treated with TNF-α/CHX, and then cell death and autophagic flux were detected. We showed that BMSCs treated with TNF-α/CHX presented dramatically elevated autophagic flux and cell death. Furthermore, we showed that 3-MA and shBECN1 treatment accelerated TNF-α/CHX-induced apoptosis, but that Rap treatment ameliorated cell death. Our results demonstrate that autophagy protects BMSCs against TNF-α-induced apoptosis. Enhancing the autophagy of BMSCs may elevate cellular survival in an inflammatory microenvironment.