Journal of Orthopaedic Surgery and Research最新文献

Introduction: Neuroblastoma is the second most common childhood malignancy. Only a minority of children with metastatic disease present initially to orthopedic surgeons, despite musculoskeletal complaints such as back pain, limb pain, limp, extremity swelling, or findings mimicking osteomyelitis. These vague and nonspecific presentations increase the risk of delayed diagnosis.

Aims: To study orthopedic manifestations that present as the initial presenting symptoms of neuroblastoma in children and to characterize their clinical, radiological, and laboratory profiles.

Materials and methods: Forty-six consecutive patients with neuroblastoma were retrospectively evaluated. Medical records were reviewed, with particular attention given to the presence of orthopedic manifestations preceding the diagnosis of neuroblastoma. The children who were presented primarily to the orthopedics department were identified. The details of musculoskeletal symptoms and radiological and laboratory investigations were analyzed.

Results: Seven children (20%) presented initially with orthopedic complaints. Three patients had spinal involvement, including paraplegia from hydromyelia or vertebral metastasis with lytic-sclerotic lesions. Three children presented with persistent hip pain and limp and were initially diagnosed with osteomyelitis before biopsy confirmed neuroblastoma. One child presented with nontraumatic forearm swelling, initially presumed as osteomyelitis, with radiographs showing lysis of the ulnar metaphysis. A biopsy was used to establish the diagnosis. Six children had severe anemia with elevated ESR and CRP, and three had markedly elevated LDH levels.

Conclusion: Approximately one-fifth of children with neuroblastoma initially present to orthopedic surgeons. Persistent or atypical musculoskeletal complaints-especially hip pain or back pain accompanied by anemia, high ESR, or high CRP-should prompt the consideration of neuroblastoma and early histopathological evaluation to avoid diagnostic delays.

Objective: No studies have been reported on the associations between the polymorphisms and mutations of rs11573819, rs2073618, and rs3102735 loci in osteoprotegerin (OPG) gene and bone metabolism in postmenopausal women in Shihezi, Xinjiang. Therefore, this study aimed to investigate the relationship between the polymorphisms and mutations of these three OPG gene loci and bone metabolism in postmenopausal women in this region.

Methods: This study enrolled 200 postmenopausal women who were divided into two groups based on the results of bone mineral density (BMD): the normal bone mineral density group (NBM group) and the low bone mineral density group (LBM group). Baseline data, biochemical indicators, BMD and other information of the subjects were collected and compared. The polymorphisms of OPG loci were determined by Matrix-Assisted Laser Desorption/Ionization Time-of-Flight Mass Spectrometry (MALDI-TOF MS).

Results: (1) Compared with the NBM group, the LBM group had higher mean age, longer menopausal years and elevated TyG index, while lower levels of HDL and BMD (L_1-4 and femoral neck). (2) At the rs2073618 locus, there was a statistically significant difference in genotype distribution between the two groups. (3) After multiple testing correction using the Benjamini-Hochberg method, at the rs11573819 locus: Compared with the GG genotype (wild type), the AA/GA genotypes (mutant type) in the NBM group had lower levels of BMD (L_1-4 and femoral neck), and the AA/GA genotypes (mutant type) in the LBM group had lower levels of BMD (femoral neck). (4) Multiple linear regression analysis: For BMD (L_1-4), the influencing factors included menopausal years, WHR, FPG, LDL, HDL, TyG index, AST, and the mutation of rs11573819 locus. For BMD (femoral neck), the influencing factors included menopausal years, LDL, HDL, and the mutation of rs11573819 locus.

Conclusion: The polymorphism of OPG gene rs2073618 locus and the mutation of OPG gene rs11573819 locus may be associated with bone metabolism in postmenopausal women in Shihezi, Xinjiang.

Introduction: Arthroscopic lateral retinacular release (LRR) is an effective treatment for lateral patellar compression syndrome (LPCS), but postoperative rehabilitation remains crucial. Low-load blood flow restriction training (LL-BFRT) has been shown to be beneficial in sports medicine; however, its effect on postoperative recovery in LPCS is unclear.

Methods: In this randomized controlled trial, 60 patients after LRR were assigned to receive either routine rehabilitation with LL-BFRT or routine rehabilitation alone for 4 weeks. Outcomes included Lysholm score, knee extension peak torque, quadriceps thickness, thigh circumference, VAS, and ROM. Within- and between-group comparisons were conducted using paired and unpaired t-tests or their non-parametric equivalents, according to data distribution and homogeneity of variance (SPSS; P < 0.05 was considered statistically significant).

Results: A total of 51 patients (Control: n = 26, age 45.3 ± 11.6 years, BMI 24.0 ± 3.1; LL-BFRT: n = 25, age 42.4 ± 10.2 years, BMI 25.2 ± 3.4) completed the trial. While both groups showed post-intervention improvements, the LL-BFRT group demonstrated greater gains than the control group in knee extensor strength at 60°/s (mean increase 20.85 vs. 8.24 N·m), vastus medialis thickness (0.33 vs. 0.12 cm), and thigh circumference (2.34 vs. 1.15 cm). Although the between-group differences in VAS and Lysholm scores were not statistically significant, the mean changes in the LL-BFRT group exceeded the minimal clinically important difference (MCID) thresholds for both outcomes (VAS: 2 cm; Lysholm: 11.1 points), indicating clinically meaningful within-group improvement.

Conclusion: LL-BFRT augments routine rehabilitation by specifically improving knee extensor strength, vastus medialis hypertrophy, and thigh circumference in patients with LPCS after LRR, and may represent an effective strategy to enhance postoperative recovery.

Background: Intervertebral disc degeneration (IDD) is closely related to the dysfunction of nucleus pulposus cells (NPCs) and the imbalance of their microenvironment. MicroRNAs play a key role in cell differentiation and homeostasis regulation, but the mechanisms underlying the differentiation of bone marrow mesenchymal stem cells (BMSCs) into NPCs are still unclear.

Methods: Using BMSCs and NPCs, this study performed qPCR to measure the expression of miR-140-5p, miR-145-5p, and cartilage-related genes; dual-luciferase reporter assays to verify miR-145-5p targeting SOX9; After inducing BMSC differentiation through miRNA, cell proliferation and migration were analyzed using CCK-8 and Transwell assays, while ELISA and oxidative stress kits were used to detect inflammation factors and oxidative stress levels.

Results: Compared to BMSCs, NPCs exhibited significantly upregulated expression of miR-140-5p, SOX9, COL2A1 and Aggrecan, alongside decreased miR-145-5p levels, reduced ROS and enhanced SOD activity. Mechanistically, SOX9 was confirmed as a direct target of miR-145-5p, while network analysis revealed its functional connection to miR-140-5p targets. Furthermore, dual miRNA modulation synergistically suppressed Notch signaling, promoting the expression of nucleus pulposus-associated markers (KRT19, CA12, HIF-1α), enhancing anabolic genes while suppressing catabolic factors. This coordinated regulation attenuated proliferation and migration while improving oxidative stress and inflammatory microenvironments, collectively promoting chondrogenic differentiation.

Conclusions: The synergistic action of miR-145-5p (via SOX9 targeting) and miR-140-5p promotes BMSC differentiation toward an NPC-like phenotype in vitro, providing mechanistic insight and identifying a potential therapeutic target for disc degeneration that requires future in vivo validation.

Open fractures of the lower extremity remain challenging to manage even in the most experienced surgical teams. These injuries when they present with bone loss pose even greater challenges with often unpredictable outcomes. Whilst traditionally, bone transport has been used as the surgical technique to treat open long bone injuries with bone loss, recently the Masquelet technique has gained great popularity amongst surgeons to manage these injuries. Understanding better the role of the induced membrane, its molecular signature (possessing angiogenic, osteogenic and inductive properties) and the capabilities that exist to improve the biological potency of the graft materials implanted, as well as appreciating the contribution of several tips and tricks that have been developed (membrane preservation and graft optimisation), good results can be expected. Additionally, it appears that from the health economic perspective, the technique is associated with less costs compared to bone transport. Herein the Masquelet technique is described for the management of open fractures of the lower extremity presenting with bone loss providing useful tips on how complications can be reduced whilst improving clinical outcomes.

Background: Osteoarthritis (OA) is a prevalent degenerative joint disorder whose pathogenesis may involve chronic inflammation. This research sought to discover new biomarkers linked to OA and to investigate their functional roles in the disease process.

Methods: Differentially expressed genes (DEGs) in OA were screened through bioinformatic analysis and subjected to Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses. An in vitro model of OA was established by inducing chondrocyte degeneration using IL-1β. Expression levels of MMP25, collagen II, and aggrecan were quantified via RT-qPCR. Cell viability and apoptosis were assessed using the CCK-8 assay and the flow cytometry, respectively.

Results: Bioinformatics analysis identified MMP25 upregulation in OA. Elevated MMP25 levels were observed in individuals with knee osteoarthritis and in IL-1β-exposed CHON-001 chondrocytes. Silencing MMP25 attenuated the IL-1β-induced reduction in chondrocyte viability and increase in apoptosis. Furthermore, knockdown of MMP25 enhanced anabolic activity related to extracellular matrix synthesis in IL-1β-stimulated chondrocytes.

Conclusion: MMP25 may serve as a potential biomarker for evaluating knee osteoarthritis and it appears to mediate IL-1β-induced chondrocyte injury and extracellular matrix degradation.

Ankylosing spondylitis (AS) is an immune-mediated disease with an unknown etiology, posing challenges in effective treatment. This study aims to investigate the underlying mechanisms and explore the potential of traditional Chinese medicine (TCM) as a treatment avenue. Employing a multiomics analysis and leveraging public databases, we scrutinized AS immune cell subpopulations and associated genes. Gene regulatory mechanisms were dissected, and molecular docking was performed to assess the therapeutic efficacy of TCM. Our findings revealed a significant elevation in effector CD8+ memory T (Tem) cells in AS. Notably, the expression of STAT4 in this cell subpopulation was observed to be down-regulated. This down-regulation might be influenced by multiple circRNAs and miR-574-5p. Intriguingly, components derived from guava leaves exhibited a stable binding affinity to STAT4. Immunohistochemistry and qPCR results confirmed low expression of STAT4 in paraspinal ligament muscle tissue. This comprehensive multiomics analysis sheds light on potential underlying mechanisms of AS and underscores the prospect of traditional Chinese medicine as a viable therapeutic option. The study provides valuable insights for future research endeavors.

Objective: Fear of falling (FOF) after ankle fracture surgery significantly hinders rehabilitation in elderly patients, yet the optimal timing for physical therapy (PT) remains debated. This study examines how PT initiation time affects FOF and functional recovery.

Methods: In this single-center retrospective cohort study, we analyzed 2,816 patients (aged ≥ 65) with ankle fractures (2014-2023), stratified into early (≤ 2 weeks post-operation) and conventional PT (>2 weeks) groups. Primary outcomes were changes in FES-I and AOFAS scores; secondary outcomes included complication rates and time to resuming daily activities. Propensity score matching controlled for confounders, and interaction analysis assessed the moderating effect of fracture type (Weber classification).

Results: At 12 months, the early PT group showed significantly lower FES-I scores (median 19 [IQR 17-23] vs. 17 [IQR 22-27], P < 0.001), and higher AOFAS scores (85.5 [78-92] vs. 77 [70-86], P < 0.001). Weber type B fractures benefited most, with early PT yielding greater FES-I improvements (2.8-point difference; 95% CI 1.8-3.8, P < 0.001) and AOFAS gains (10.0 points; 95% CI 8.4-11.6, P < 0.001). Complication rates were similar (9.2% early vs. 11.8% conventional, P = 0.078), but early PT had lower deep vein thrombosis incidence (3.5% vs. 5.7%, P = 0.035).

Conclusion: Early PT significantly reduces FOF and enhances functional recovery, particularly in Weber type B fractures. We recommend individualized PT protocols based on fracture type and bone density.

Trial registration: Retrospectively registered.

Background: Rotator cuff (RC) repairs heal unreliably, particularly in chronic disease. The molecular mechanisms underlying failed repair remain poorly understood. While individual studies have examined protein expression in diseased RC tissue, no synthesis has investigated these findings across various disease stages. This systematic review explores the stage-specific protein expression of human RC degeneration using immunohistochemistry.

Methods: Following PRISMA guidelines, MEDLINE, Embase, and Cochrane Library were systematically searched to September 2025 for human studies that use immunohistochemistry to evaluate protein expression in intraoperative RC tendon or muscle biopsies. Study quality was appraised with Joanna Briggs Institute (JBI) tools. No meta-analysis was performed due to heterogeneity.

Results: Forty-seven studies were included. Despite methodological heterogeneity, convergent molecular patterns emerged within disease stages. Partial and small tears demonstrated hypoxic-inflammatory-apoptotic signatures (HIF-1α, BNip3, IL-6, IL-1β, MMP-1/3/9) with preserved regenerative markers (Ki67, CD34), suggesting reparative potential. Medium tears exhibited sustained angiogenic activity (VEGF) and emerging adipogenic drift (PPARγ, C/EBPα). Large and massive tears showed depletion of anabolic factors (TGF-β1, BMP-5), M2-macrophage predominance (CD206, CD163), and fibrofatty infiltration. Patient comorbidities (diabetes, vitamin D deficiency, smoking) amplified inflammatory and adipogenic signatures.

Conclusions: Cross-sectional human immunohistochemical evidence infers a stage-associated molecular trajectory: inflammatory-hypoxic stress with retained reparative capacity at earlier disease stages to fibrotic-adipogenic failure at later stages. This molecular framework may support future approaches to surgical decision-making and precision therapies.