Background: Rotator cuff tears (RCTs) are culprit of shoulder pain and dysfunction. Tendon-bone interface (TBI) mal-healing is an essential contributor to retear after RCTs. Consequently, present project was conducted to investigate the role of bone marrow mesenchymal stem cells (BMSCs)-derived exosomes on TBI healing. Method: Young BMSCs (Y-BMSCs) and Aged BMSCs (A-BMSCs) were isolated from Young (3-month-old) and old (24-month-old) SD rats, and their-derived exosomes (A-BMSCs-exo and Y-BMSCs-exo) were identified. RCTs model was established, and A-BMSCs-exo and Y-BMSCs-exo were injected at the rotator cuff using hydrogel as a vehicle. Pathological changes of TBI were observed by HE, Sirius Red and Oil Red O staining. Western blotting and RT-qPCR were applied to assess the expression of extracellular matrix (ECM)-, tendon cell (TCs)-, osteogenic-, tendon-derived stem cell (TDSCs)- and angiogenic-associated proteins and mRNAs in TBI. Result: Y-BMSCs exhibited increased activity, osteogenic and lipogenic abilities than A-BMSCs. After A-BMSCs-exo and Y-BMSCs-exo treatment, TBI displayed massive sharpey’s fibers growing along the tendon longitudinally, and a collagen fiber-chondrocyte migration zone forming a typical tendon-noncalcified fibrocartilage-calcified fibrocartilage-bone structure. A-BMSCs-exo and Y-BMSCs-exo significantly upregulated the expression of collagen Col I/II/III, Aggrecan, TNMD, SCX, Runx2, OPN, CD45, Sox2, CD31 and VEGFR2 in TBI. In vitro, A-BMSCs-exo and Y-BMSCs-exo significantly enhanced the activity of TCs and TDSCs, TDSCs stemness, and reduced the osteogenic and lipogenic capacity of TDSCs. The effect of Y-BMSCs-exo was significantly stronger than that of A-BMSCs-exo. Conclusion: BMSCs-derived exosomes facilitate ECM remodeling, osteogenic differentiation, angiogenesis, and stemness of TDSCs, thereby accelerating TBI healing in RCTs, with better outcomes using young individual-derived BMSCs.

Background: Low back pain (LBP) is a common chief complaint from athletes. Lumbar spondylolysis (LS) is a common sport injury. Severe LS is likely to cause spinal instability, resulting in lumbar spondylolisthesis or lumbar disc herniation, and even damage to the spinal nerve roots. The incidence of LS is approximately 5% in the adult population, and nearly half of young athletes with LBP are diagnosed with LS. This meta-analysis analyzed the incidence of LS in athletes with LBP. Methods: PubMed, Embase, Cochrane (Cochrane Central Register of Controlled Trials), and Web of Science databases were systematically searched for published case report and retrospective analyses related to the topic from the date of database creation to January 1,2023. Relevant literature was screened and information extracted, and risk of bias was assessed for included studies using the methodological index for non-randomized-studies scale. Single-arm Meta-analysis was performed using R4.04 software. Heterogeneity was quantified by Cochran Q test and Higgins I ². Funnel plots were used to visualize publication bias, and Egger test and Begg test were used to statistical tests. Results: A total of 9 studies (835 patients) were included in this study. Meta-analysis revealed that the prevalence of LS in athletes with LBP was estimated at 41.7%, [95% CI = (0.28–0.55)], but this prevalence varied considerably with the gender and age of the athletes. Conclusion: The estimated prevalence of LS in athletes with LBP is 41.7%, and future correlations between the prevalence of LS in adolescent athletes worldwide need to be assessed from different perspectives, including biomechanical, hormonal, anatomical, behavioral, and gender differences.

Osteomyelitis is one of the most challenging diseases in the field of orthopedics for its complex pathogenesis and unsatisfactory treatment. The mechanism underlying its occurrence and development is still unclear. In our previous study, we found that long non-coding RNA (lncRNA) NONHSAT009968 inhibited the ability of osteogenic differentiation in staphylococcal protein A (SPA)-treated human bone marrow mesenchymal stem cells (hBMMSCs), but the underlying mechanism remains unclear. The current study was aimed at elucidating the possible mechanism of NONHSAT009968 in regulating osteogenic differentiation and bone defect repairability of hBMMSCs under infection. It was revealed that Wnt3a played a key role in promoting osteogenic differentiation of hBMMSCs treated with SPA in vitro. In addition, NONHSAT009968 inhibited osteogenic differentiation of hBMMSCs treated with SPA via Wnt3a, both in vivo and in vitro. In sum, the results suggested that lncNONHSAT009968 inhibited osteogenic differentiation of hBMMSCs in SA-induced inflammation through Wnt3a, which may have affected the occurrence and development of osteomyelitis. This study might provide novel insights regarding osteomyelitis and infectious bone defects.

Background: To elucidate the differences in mechanical performance between a novel axially controlled compression spinal rod (ACCSR) for lumbar spondylolysis (LS) and the common spinal rod (CSR). Methods: A total of 36 ACCSRs and 36 CSRs from the same batch were used in this study, each with a diameter of 6.0 mm. Biomechanical tests were carried out on spinal rods for the ACCSR group and on pedicle screw-rod internal fixation systems for the CSR group. The spinal rod tests were conducted following the guidelines outlined in the American Society for Testing and Materials (ASTM) F 2193, while the pedicle screw-rod internal fixation system tests adhered to ASTM F 1798-97 standards. Results: The stiffness of ACCSR and CSR was 1559.15 ± 50.15 and 3788.86 ± 156.45 N/mm (P < .001). ACCSR’s yield load was 1345.73 (1297.90–1359.97) N, whereas CSR’s was 4046.83 (3805.8–4072.53) N (P = .002). ACCSR’s load in the 2.5 millionth cycle of the fatigue four-point bending test was 320 N. The axial gripping capacity of ACCSR and CSR was 1632.53 ± 165.64 and 1273.62 ± 205.63 N (P = .004). ACCSR’s torsional gripping capacity was 3.45 (3.23–3.47) Nm, while CSR’s was 3.27 (3.07–3.59) Nm (P = .654). The stiffness of the pedicle screws of the ACCSR and CSR group was 783.83 (775.67–798.94) and 773.14 (758.70–783.62) N/mm (P = .085). The yield loads on the pedicle screws of the ACCSR and CSR group was 1345.73 (1297.90–1359.97) and 4046.83 (3805.8–4072.53) N (P = .099). Conclusion: Although ACCSR exhibited lower yield load, stiffness, and fatigue resistance compared to CSR, it demonstrated significantly higher axial gripping capacity and met the stress requirement of the human isthmus. Consequently, ACCSR presents a promising alternative to CSR for LS remediation.

Increasing evidence suggests that ferroptosis plays a pivotal role in Staphylococcus aureus (S. aureus)-induced osteomyelitis. However, the regulatory mechanisms underlying ferroptosis-related genes (FRGs) in osteomyelitis remain poorly understood. This study aimed to identify key FRGs and elucidate their regulatory roles in osteomyelitis. Key FRGs were identified using least absolute shrinkage and selection operator (LASSO) logistic regression and support vector machine-recursive feature elimination (SVM-RFE) algorithms based on transcriptomic data from the Gene Expression Omnibus (GEO) database. Bone marrow mesenchymal stromal cells (BMSCs) were isolated, characterized, and infected with S. aureus protein A (SpA) to construct an in vitro model. Cell viability, osteogenic differentiation, inflammation, and gene expression were assessed using Cell Counting Kit-8 (CCK-8), Alizarin Red S staining, enzyme-linked immunosorbent assay (ELISA), and quantitative reverse transcription polymerase chain reaction (qRT-PCR). In vivo, a mouse model of S. aureus-induced osteomyelitis was established, and the role of KLF2 was examined by micro-computed tomography (micro-CT), ELISA, histological staining, immunohistochemistry, immunofluorescence, and qRT-PCR. A total of 683 differentially expressed FRGs were identified. Ten candidate biomarkers were screened using LASSO and SVM-RFE, of which TXN, KLF2, HSPA8, CCT3, and AKR1C3 were consistently validated across training and validation datasets. These genes were associated with immune regulation, protein synthesis, and multiple ribosome- and metabolism-related pathways. In vitro, SpA treatment increased inflammation response, reduced BMSC proliferation and osteogenic differentiation, upregulated HSPA8, TXN, and CCT3, and downregulated KLF2 and its putative downstream target GPX4. In vivo, KLF2 overexpression alleviated S. aureus-induced bone loss, inflammation, and ferroptosis, while promoting angiogenesis and osteogenesis, in part through modulation of GPX4. This study highlights KLF2 as a potential protective factor in S. aureus-induced osteomyelitis, possibly by regulating GPX4 and ferroptosis.