Background Although cervical intervertebral disc (IVD) degeneration is closely associated with neck pain, its cause remains unclear. In this study, an animal model of cervical disc degeneration and discogenic neck pain induced by a low concentration of Propionibacterium acnes ( P. acnes -L) is investigated to explore the possible mechanisms of cervical discogenic pain. Methods Cervical IVD degeneration and discitis was induced in 8-week-old male rats in C3–C6 IVDs through the anterior intervertebral puncture with intradiscal injections of low and high concentrations of P. acnes ( P. acnes -L, n = 20 and P. acnes -H, n = 15) or Staphylococcus aureus ( S. aureus , n = 15), compared to control (injection with PBS, n = 20). The structural changes in the cervical IVD using micro-CT, histological evaluation, and gene expression assays after MRI scans at 2 and 6 weeks post-modeling. The P. acnes -L induced IVD degeneration model was assessed for cervical spine MRI, histological degeneration, pain-like behaviors (guarding behavior and forepaw von Frey), nerve fiber growth in the IVD endplate region, and DRG TNF-α and CGRP. Results IVD injection with P. acnes -L induced IVD degeneration with decreased IVD height and MRI T2 values. IVD injection with P. acnes -H and S. aureus both lead to discitis-like changes on T2-weighted MRI, trabecular bone remodeling on micro-CT, and osseous fusion after damage in the cartilage endplate adjacent to the injected IVD. Eventually, rats in the P. acnes -L group exhibited significant nociceptive hypersensitivity, nerve fiber ingrowth was observed in the IVD endplate region, inflammatory activity in the DRG was significantly increased compared to the control group, and the expression of the pain neurotransmitter CGRP was significantly upregulated. Conclusion P. acnes -L was validated to induce cervical IVD degeneration and discogenic pain phenotype, while P. acnes -H induced was identified to resemble septic discitis comparable to those caused by S. aureus infection.

Background:Intervertebral disc degeneration (IVDD) is a major cause of low back pain and imposes a significant burden on individuals and society. Bioactive materials are widely used for tissue repair. Here, we designed a calcium alginate (Alg-Ca2⁺) modified with N, N-dimethylaminoethyl methacrylate (DMAEMA) and acrylamide (AAm), named AAm-DMAEMA/Alg-Ca2⁺, and evaluated its effects on IVDD repair. Methods:Morphology of AAm-DMAEMA/Alg-Ca2⁺ (referred to as AAm) was analyzed by SEM. IVDD was induced in rats via Co6/7 and Co7/8 disc puncture, followed by AAm treatment. Disc height, tissue integrity, and matrix composition were assessed by X-ray, MRI, HE, and Safranin O staining. Aggrecan, collagen I/II, MMP3/13, and Ki-67 were analyzed by immunohistochemistry and immunofluorescence. NP cells exposed to H2O2 were used to model inflammation in vitro; cell viability, proliferation, and inflammatory factor expression were measured by CCK-8, EdU, qPCR, and immunofluorescence (IF) assays. Results:AAm treatment significantly enhanced the viability and proliferation of NP cells by almost 50% percent. AAm treatment notably alleviated disc height loss, restored tissue integrity, and increased the DHI value in rat model. MRI images showed that while the endplate signal was decreased in the model group, AAm treatment increased the signal at 4 and 8 weeks post-modeling. AAm mitigated disc height loss, improved MRI signals, preserved nucleus pulposus structure, reduced fibrous tissue formation, and promoted bone formation and chondrogenesis. AAm treatment repressed the levels of TNF-α, IL-1, IL-6, and NLRP3 in NP cells. H2O2 induction suppressed the levels of Aggrecan and collagen II and elevated MMP3 and MMP13 expression in NP cells, effects that were reversed by the administration of AAm. Conclusion:AAm treatment facilitates the proliferation of NP cells, represses the inflammatory response, alleviates tissue damage, and enhances bone formation in IVDD. These results indicate that AAm-DMAEMA/Alg-Ca2+ hydrogel is a promising bioactive scaffold for promoting IVDD.

The management of critical-sized bone defects has attracted heightened interest due to its challenging nature. To date, numerous engineered tissues incorporating nano-hydroxyapatite (nHap) have been proposed; however, nHap continues to encounter limitations, particularly regarding its inadequate immunomodulatory effects on bone. Therefore, needlelike nHap (NnHap)-based scaffolds were fabricated using a polylactic acid derivative and carboxymethyl chitosan. We hypothesize that NnHap@CP can not only promote bone immunomodulatory effects and angiogenesis in human umbilical vein endothelial cells through M2 subtype polarization but also directly promote osteogenesis in rat bone-marrow-derived mesenchymal stem cells (rBMSCs). Furthermore, mass spectrometry was employed to determine that osteoprotegerin/RANK/RANKL may represent a potential signaling pathway through which NnHap@CP enhances the osteogenesis of rBMSCs. In our study, NnHap@CP demonstrated a satisfactory effect on M2 subtype polarization in macrophages and enhanced osteogenesis in rBMSCs, as observed in an in vitro study. We employed NnHap@CP for the in vivo examination of a rat model with cranial critical-sized bone defects. We discovered that NnHap@CP significantly enhances new bone regeneration and neovascularization, potentially serving as an innovative treatment strategy for critical bone defects.

Objective:The rising prevalence of obesity has raised concerns about its impact on surgical outcomes. Obesity is a critical risk factor of low back pain and lumbar degeneration diseases, but it is still unclear whether obesity is related to lumbar surgical outcomes in the Chinese population. This study examines the influence of body mass index (BMI) on the clinical effectiveness of lumbar decompression surgery in patients with lumbar canal stenosis (LCS). Methods:465 patients with single-segment LCS treated with lumbar decompression surgery at the LiHuiLi Hospital between April 2018 and August 2023 were enrolled in this study. Patients were divided into obesity (OB, BMI > 30 kg/m²) and non-obesity (NOB, BMI < 24 kg/m²) groups. Baseline data, operation time (OT), hospital stay (HS), Visual Analogue Scale (VAS) scores, Oswestry Disability Index (ODI), and maximum walking distance (MWD), C-reaction protein (CRP), white blood cell (WBC), complications, and reoperations were evaluated. Results:Of the total participants, 156 were categorized as OB and 309 as NOB. The NOB group exhibited significantly greater improvement in VAS scores at 1 month and ODI scores at 3 and 12 months postoperatively (P < 0.001). The OB group had significantly lower MWD both preoperatively and at the final follow-up compared to the NOB group (P < 0.001). The OB group also had significantly longer OT and HS (P < 0.001), as well as higher rates of complications and reoperations compared to the NOB group (P < 0.05). Linear regression revealed a significant relationship between BMI and MWD (P < 0.001). Conclusions:Obesity maybe associated with poorer functional recovery, increased complications, and prolonged recovery following lumbar decompression surgery.

ObjectiveThis study aimed to identify novel diagnostic genetic biomarkers for early-stage cervical intervertebral disc degeneration (IDD) and to investigate the potential relationship between key genes and immune cell infiltration in IDD.MethodsmRNA expression profiles were obtained from the Gene Expression Omnibus (GEO) database. Differentially expressed genes (DEGs) between cervical IDD and control samples were identified using the linear model (limma R package). Functional annotation and pathway enrichment analyses were performed with Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG). A Least Absolute Shrinkage and Selection Operator (LASSO) regression model and Support Vector Machine–Recursive Feature Elimination (SVM-RFE) were applied to screen potential biomarkers. Immune cell composition in IDD samples was estimated using the CIBERSORT method. Cervical disc specimens were collected from patients undergoing anterior cervical discectomy and fusion (ACDF) and classified into IDD and control groups based on MRI Pfirrmann grading. Quantitative PCR (qPCR) was performed to validate biomarker expression in these specimens.ResultsA total of 71 DEGs were identified, including 50 upregulated and 21 downregulated genes in IDD samples. KEGG pathway analysis revealed significant enrichment in inflammation-related pathways. Through machine learning screening and experimental validation, we identified CDKN3, SLC22A4, and SYDE1 as key diagnostic biomarkers for IDD. Immune infiltration analysis suggested that these genes may contribute to IDD pathogenesis by modulating specific immune cell populations. qPCR results confirmed that CDKN3 expression was significantly downregulated in cervical IDD specimens (P < 0.05), whereas SLC22A4 and SYDE1 were significantly upregulated (P < 0.05).ConclusionCDKN3, SLC22A4, and SYDE1 are associated with the pathogenesis and progression of cervical IDD, potentially through their regulatory effects on immune cell activity. These genes may serve as promising diagnostic biomarkers for cervical IDD and could aid in monitoring disease progression. Further studies are warranted to validate their clinical utility and elucidate the underlying mechanisms.

Substantial vascularization has emerged as a promising tissue engineering strategy for regenerating critical-sized bone defects. In this study, we developed an injectable smart hydrogel system (GH-LR) by incorporating roxadustat (RD)-loaded MgFe-layered double hydroxide nanoparticles into a gelatin methacryloyl/hyaluronic acid methacrylate (GH) hybrid matrix. This bioactive composite enables the sustained release of therapeutic agents (RD, Mg2+, and Fe3+), synergistically promoting angiogenesis-osteogenesis coupling. Comprehensive characterization confirmed the successful synthesis of GH-LR hydrogels with efficient drug encapsulation. In vitro studies demonstrated that GH-LR significantly enhanced endothelial tube formation in human umbilical vein endothelial cells and osteogenic differentiation in bone marrow mesenchymal stem cells (BMSCs), attributable to the prolonged release of bioactive molecules. Mechanistic investigations using RNA sequencing revealed activation of the PI3K-Akt pathways in BMSCs treated with GH-LR hydrogels, correlating with enhanced osteogenesis. In vivo, evaluation in a critical-sized calvarial defect model confirmed accelerated bone regeneration, as evidenced by upregulated expression of Runx2 and Col-1. The therapeutic effects stem from the synergistic interplay between locally sustained angiogenesis and osteogenesis induction. This biocompatible GH-LR system collectively represents an innovative approach for reconstructing large bone defects through controlled delivery and spatiotemporal coordination of pro-regenerative cues.

As a chronic joint disease, osteoarthritis (OA) severely impairs patients’ quality of life and mobility. The deubiquitinating enzyme USP14 and Cadherin-11 (CDH11) have been implicated in OA pathogenesis. However, the regulatory interplay between them remains poorly defined. IL-1β was used to stimulate chondrocytes for in vitro OA model establishment. Bioinformatics database was employed to assess CDH11 expression in OA samples. MTT assay was performed to evaluate cell viability. Protein expression was analyzed via Western blot. Cell apoptosis was detected by flow cytometry. Levels of ROS, GSH, MDA, Fe2+, as well as concentrations of TNF-α and IL-6, were measured using respective assay kits. CDH11 expression was upregulated in OA samples and IL-1β-induced chondrocytes. Moreover, silencing CDH11 promoted cell viability and attenuated cell apoptosis, inflammation, oxidative stress, and ferroptosis. USP14 stabilized CDH11 through deubiquitination, sustaining CDH11-mediated chondrocyte damage. After USP14 knockdown, cell viability was increased, while cell apoptosis, inflammation, oxidative stress and ferroptosis were mitigated. Furthermore, CDH11 overexpression abrogated the effects of USP14 knockdown on IL-1β-stimulated chondrocytes. USP14 mediates IL-1β-induced chondrocyte injury by stabilizing CDH11 through deubiquitination, highlighting the USP14-CDH11 axis as a potential regulatory pathway in OA-related chondrocyte pathology.

[This corrects the article DOI: 10.3389/fmed.2025.1729401.].

BACKGROUND:Anterior cruciate ligament reconstruction (ACLR) is the dominant clinical modality for the treatment of anterior cruciate ligament injuries. The success of ACLR is largely dependent on tendon-bone healing, and stem cell biotherapies are often used to facilitate this process. Histone lactylation modifications are involved in the regulation of various diseases. Lactate dehydrogenase A (LDHA) has been shown to play an important role in exosomes. AIM:To explore the regulation of tendon-bone healing after ACLR by LDHA in exosomes derived from bone marrow mesenchymal stem cells (BMSC-Exos). METHODS:BMSC-Exos and LDHA were characterized and analyzed by transmission electron microscopy, qNano, immunofluorescence and western blotting assay. The corresponding low expression cell lines were obtained using RNA interference transfection; LDHA expression in rat bone tissues after ACLR was analyzed by western blotting. The volume of newborn bone tissues was monitored by micro-computed tomography imaging. Tendon and fibrocartilage regeneration were further analyzed and calculated by histological analysis, including hematoxylin and eosin and Safranin O-Fast green staining, respectively; LDHA levels of chondrocyte stem cells (CSPCs) after co-incubation with BMSC-Exos were analyzed by western blotting. Extracellularly secreted lactic acid content was determined by lactate assay kit. Cell viability was assessed by cell counting kit 8 assay, and the proliferation and differentiation ability of cells was further examined by the expression of collagen II, SOX9 and aggrecan. Histone H3K18 lactylation modification was analyzed by western blotting. H3K18 La binding on bone morphogenetic protein 7 (BMP7) promoter was analyzed by chromatin immunoprecipitation-quantitative polymerase chain reaction; BMP7 promoter activity was analyzed by dual luciferase reporter gene; BMP7 protein expression was analyzed using quantitative polymerase chain reaction and western blotting. Then, the proliferation of CSPCs promoted by BMSC-Exos LDHA was analyzed by protein expression levels of LDHA, BMP7, collagen II, SOX9, aggrecan, extracellular lactate content, and cell counting kit 8 assay. RESULTS:The spherical nanosized BMSC-Exos could be uptaken by CSPCs. LDHA was highly expressed in BMSC-Exos, which could infiltrate into the bone tissue of ACLR rats and promoted the generation of new bone tissue, as well as significantly increased the regeneration of tendon and fibrocartilage. Co-incubation of CSPCs with high-expressing LDHA BMSC-Exos increased the secretion of lactate content from CSPCs, cell viability, and the expression of markers related to cell proliferation and differentiation, including collagen II, SOX9, and aggrecan; LDHA in BMSC-Exos upregulated BMP7 through histone H3K18 lactate modification; high LDHA expression reversed the knockdown of BMP7, further increasing the proliferation and differentiation of CSPCs, thereby inducing cartilage formation. CONCLUSION:LDHA in BMSC-Exos promotes BMP7 expression via H3K18 lactylation modification, which further promotes tendon-bone healing after ACLR.

Introduction:Osteoarthritis (OA) is a common chronic joint disease that severely affects patients' quality of life. Quercetin, a natural flavonoid, exhibits chondroprotective effects, though its bioavailability through regular oral consumption is limited. In this study, we employed two-dimensional MXene nanosheets as a nanocarrier to facilitate targeted intracellular delivery of quercetin, aiming to enhance its therapeutic efficacy against OA. Methods:Methods: Porous Ti₃C₂Tₓ MXene nanosheets were synthesized via selective etching and then loaded with quercetin through physical adsorption. Material characterization was performed using transmission electron microscopy (TEM), scanning electron microscopy (SEM), ultraviolet-visible spectroscopy (UV-Vis), dynamic light scattering (DLS), and in vitro release assays. For in vitro evaluation, IL-1β-stimulated primary mouse articular chondrocytes (ACs) were treated with free quercetin or MXene-loaded quercetin, followed by assessments of cell viability, apoptosis, cell cycle progression, migration, oxidative stress markers, and ferroptosis-related protein expression. For in vivo validation, a destabilization of the medial meniscus (DMM) mouse model of OA was established to assess cartilage morphology, ferroptosis markers, and histological changes after intra-articular injection of treatments. Results:MXene-loading significantly enhanced quercetin's protective effects in IL-1β-induced primary mouse ACs, including improved cell viability and proliferation, reduced apoptosis, alleviated oxidative stress, and suppression of ferroptosis. In OA mice, MXene-quercetin treatment more effectively preserved cartilage integrity and inhibited ferroptosis compared with free quercetin. Conclusion:These findings suggest that MXene can serve as a biocompatible carrier to improve quercetin delivery in osteoarthritis models, supporting its potential for further preclinical evaluation.

Anoxia remains a challenging problem to effective graft implantation in bone tissue engineering for managing large-size bone defects. One promising strategy is to provide immediate oxygen required for cell viability and graft maturation by introducing oxygen-generating biomaterials. In this study, we present a novel composite oxygen-generating scaffold by integrating oxygen-generating microspheres (OMs) comprised of emulsified calcium peroxides (CPOs) encapsulated in poly (lactic-co-glycolic acid; PLGA) into the gelatin methacryloyl (GelMA) hydrogel. The in vitro results reveal that the scaffold encapsulating 2% (w/v) OMs (OM@GelMA) mildly sustained oxygen production for approximately 16 days, and hence, established hypoxic niches with low oxygen tension (10–46 mmHg) under anoxic culture condition (0.2% oxygen) for the viability of bone marrow-derived mesenchymal stem cells (BMSCs) and their enhanced osteogenic differentiation, which may be induced by activation of HIF-1/β-catenin signaling pathway by the compatibly hypoxic level as one of the underlying molecular mechanisms verified via transcriptome sequencing, western blotting (WB) and quantitative real-time polymerase chain reaction (qRT-PCR) tests on in vitro samples. Moreover, the oxygen-generating hydrogel could enhance angiogenesis of human umbilical vein endothelial cells (HUVECs) under anoxia by preserving cell viability, accelerating cell migration, promoting tube formation and activating angiogenic genes and proteins expression. In vivo studies using rat cranial critical-size defect models demonstrated that OM@GelMA significantly enhanced bone regeneration, effectively promoting bone defect repair. In summary, the OM@GelMA, as a novel endogenously oxygen-generating scaffold, holds great potential to facilitate bone tissue regeneration subject to oxygen-deprived scenarios. This study provides a new insight for future research and clinical applications in bone tissue engineering, particularly for large bone defect repair.

IntroductionThe natural polysaccharide-based injectable hydrogels have showed significant interest to use as 3D scaffolds for critical-sized bone defect repair.MethodsHere, we incorporated ZnO nanoparticles (NPs) into a newly synthesized water-soluble phosphocreatine-functionalized chitosan (CSMP) water solution to form an injectable hydrogel (CSMP-ZnO) via supramolecular combination between phosphate groups in CSMP and Zinc in ZnO NPs.ResultsThe phosphocreatine in this hydrogel not only provides sites to combine with ZnO NPs form supramolecular binding but also serves as the reservoir to control Zn2+ release. The results show that the lyophilized CSMP-ZnO hydrogels presented a porous structure with some small holes in the pore wall, as shown by scanning electron microscopy. Rheological characterizations revealed that the mechanical properties of the hydrogels were almost maintained upon the addition of ZnO NPs. In vitro experiments showed that the CSMP-ZnO hydrogel exhibits excellent angiogenic and osteogenic properties compared with the CSMP hydrogel. The as-released Zn2+ ions promote the high expression of osteoblast collagen 1 proteins and accelerate bone mineralization by activating the BMP2/SMAD signaling pathway. In vivo, the as-released Zn2+ ions promot osteoblastic proliferation and the mineralization of osteoblasts inside the CSMP-ZnO scaffolds. Immunofluorescence for RUNX2, COL-1, and CD31, showed that stable vasculature could be formed inside the CSMP-ZnO scaffolds.DiscussionBoth the in vitro and in vivo results demonstrate that CSMP-ZnO hydrogel shows promise for bone regeneration, suggesting a new strategy for tissue engineering and regeneration in the future.

This study proposes an automated neurofibroma detection method for whole-body magnetic resonance imaging (WBMRI) based on radiomics and ensemble learning. A dynamic weighted box fusion mechanism integrating two dimensional (2D) object detection and three dimensional (3D) segmentation is developed, where the fusion weights are dynamically adjusted according to the respective performance of the models in different tasks. The 3D segmentation model leverages spatial structural information to effectively compensate for the limited boundary perception capability of 2D methods. In addition, a radiomics-based false positive reduction strategy is introduced to improve the robustness of the detection system. The proposed method is evaluated on 158 clinical WBMRI cases with a total of 1,380 annotated tumor samples, using five-fold cross-validation. Experimental results show that, compared with the best-performing single model, the proposed approach achieves notable improvements in average precision, sensitivity, and overall performance metrics, while reducing the average number of false positives by 17.68. These findings demonstrate that the proposed method achieves high detection accuracy with enhanced false positive suppression and strong generalization potential.

Composite biomaterial systems facilitate regenerative medicine through component synergy. Herein, novel core-shell nanocomposites (N-HMMs) are prepared, with hollow mesoporous silica (HMSNs) as the core and magnesium-gallic acid metal-organic frameworks (Mg-MOFs) as the shell. N-HMMs are loaded with the small-molecule osteoinductive drug naringin (Nar) to form N-HMMs@Nar, which is integrated into methacrylate gelatin/polyethylene glycol diacrylate hydrogels (GelMA/PEGDA, GP) to construct N-HMMs@Nar@GP. N-HMMs@Nar@GP enables sustained release of Nar, bioactive Mg2+, and antioxidant gallic acid for synergistic anti-inflammation, osteogenesis, and angiogenesis of bone regeneration. GP adapts N-HMMs@Nar to the traumatic characteristics of bone defects and facilitates in situ treatments. In vitro studies have confirmed the composite materials' biocompatibility, osteoinductive differentiation, and angiogenesis capabilities. The ability of N-HMMs@Nar@GP to enhance osteogenesis and angiogenesis is demonstrated in an in vivo tibial defect model using micro-CT and histopathological analysis. Therefore, N-HMMs@Nar@GP holds significant potential for application in the repair of bone defects.

Purpose:To perform a meta-analysis to compare the clinical outcomes and failure rate of anterior cruciate ligament (ACL) repair and ACL reconstruction in acute ACL rupture. Methods:Studies were searched on PubMed, Web of Science, and EMBASE for randomized controlled trials comparing ACL repair versus ACL reconstruction for ACL rupture. The bias risk was based on the Cochrane Handbook for Systematic Reviews of Interventions. Clinical outcomes included IKDC score, Lysholm score, Tegner score, anteroposterior (AP) knee laxity, and failure rate. The funnel plots were used to detect publication bias. Results:Six randomized controlled study (RCTs) were included in this meta-analysis, involving a total of 478 patients. The mean follow-up varied from 1 to 5 years. The mean age of patients was between 17 and 29.1 years, the mean time from injury to surgery was 13-39 days. We found no statistical differences between ACL repair and ACLR in IKDC score (0.11; 95% CI, -0.17 to 0.40; p = 0.440; I 2 = 56.8%), Lysholm score (0.16; 95% CI, -0.10 to 0.42; p = 0.214; I 2 = 28.8%), Tegner score (0.05; 95% CI, -0.23 to 0.34; p = 0.719; I 2 = 0.0%), AP knee laxity (0.05; 95% CI, -0.17 to 0.27; p = 0.636; I 2 = 0.0%), and failure rate (RR, 1.10; 95% CI, 0.70-1.72; p = 0.695; I 2 = 27.3%). Conclusion:ACL repair showed similar clinical outcomes compared with ACLR, and it could replace ACLR as an appropriate surgical method for acute proximal ACL rupture, but the indication and selection of patients are essential to be considered. Large numbers and more high-quality studies are still needed in the future to verify our results. Level of Evidence:Level I.

AIMS:The aim of this study is to provide a detailed description of cases combining bridging patch repair with artificial ligament "internal brace" reinforcement to treat irreparable massive rotator cuff tears, and report the preliminary results.METHODS:This is a retrospective review of patients with irreparable massive rotator cuff tears undergoing fascia lata autograft bridging repair with artificial ligament "internal brace" reinforcement technique between January 2017 and May 2018. Inclusion criteria were: patients treated arthroscopically for an incompletely reparable massive rotator cuff tear (dimension > 5 cm or two tendons fully torn), stage 0 to 4 supraspinatus fatty degeneration on MRI according to the Goutallier grading system, and an intact or reparable infraspinatus and/or subscapularis tendon of radiological classification Hamada 0 to 4. The surgical technique comprised two components: first, superior capsular reconstruction using an artificial ligament as an "internal brace" protective device for a fascia lata patch. The second was fascia lata autograft bridging repair for the torn supraspinatus. In all, 26 patients with a mean age 63.4 years (SD 6.2) were included.RESULTS:All patients underwent more than two years of follow-up (mean 33.5 months (24 to 45)). All clinical scores were also improved at two-year follow-up (mean visual analogue scale 0.7 (SD 0.5) vs 6.1 (SD 1.2); p < 0.001; mean American Shoulder and Elbow Surgeons score 93.5 (SD 5.3) vs 42.5 (SD 10.8); p < 0.001; mean University of California, Los Angeles score, 31.7 (SD 3.7) vs 12.0 (SD 3.1); p < 0.001; and mean Constant-Murley score 88.7 (SD 3.5) vs 43.3 (SD 10.9); p < 0.001), and 24 of 26 fascia lata grafts were fully healed on MRI (92%). One patient had haematoma formation at the harvesting side of the fascia lata at two days postoperatively.CONCLUSION:The fascia lata autograft bridging repair combined with artificial ligament internal brace reinforcement technique achieved good functional outcomes, with a high rate of graft healing at two-year follow-up. Although the short-term results are promising, further studies with a greater number of patients would provide clearer results. Cite this article: Bone Joint J 2021;103-B(10):1619-1626.

Glucocorticoid-induced osteoporosis (GIOP) is the common reason for secondary osteoporosis. Dendrobine (DEN) is the major biologically active component of Dendrobium officinale with anti-inflammatory and antiaging properties. Whether DEN could alleviate osteogenic inhibition in GIOP rats is still unknown. The influence on osteogenic function caused by DEN on dexamethasone-treated bone marrow mesenchymal stem cells and rats was observed. The in vitro results showed that DEN reversed the inhibition of osteogenic differentiation by dexamethasone. Moreover, DEN supplementation attenuated dexamethasone-induced bone loss in vivo. DEN activated JNK and p38 MAPK pathways and restrained GR nuclear translocation, which could be prevented by the JNK (SP600125) or p38 (SB203580) pathway inhibitor. This study verified that DEN alleviated dexamethasone-induced nuclear translocation of GR, and inhibition of osteogenesis via JNK and p38 pathways, laying the foundation for DEN as a therapeutic agent for GIOP.

The primary diagnostic method for distal radius fractures remains conventional X-ray imaging. In emergency situations, rapid assessment and decision-making are often required from non-orthopedic physicians or junior radiologists in the emergency room. Therefore, an accurate and efficient auxiliary diagnostic technology for distal radius fractures is of great significance. This paper combines deep learning with image analysis techniques to propose an effective classification method for types of distal radius fractures. Firstly, an extended U-Net three-level cascade segmentation network is used for precise segmentation of the most critical joint surface and non-joint surface areas for fracture identification. The edge is further optimized using the central pixel image block classification method. Then, fracture identification is performed separately on the joint surface and non-joint surface areas. Finally, based on the classification results of the two types of images, a comprehensive judgment is made to determine normal or ABC fracture types. The experimental X-ray data comes from three tertiary hospitals, with a total of 12,000 images in the training set, 3,000 of each type, and 1,200 images in the test set, 300 of each type. To further demonstrate the generalization performance of the classification experiment, an additional 500 images were added for fracture classification testing, coming from collaborative medical institutions in the United States and Germany. All images were annotated by orthopedic medical experts with more than ten years of experience. The accuracy rates for normal, type A, type B, and type C fractures in the test set were 0.99, 0.92, 0.91, and 0.82, respectively. For orthopedic medical experts, the average recognition accuracy rates were 0.98, 0.90, 0.87, and 0.81. The proposed automatic recognition method overall performs better than experts and can be used for preliminary auxiliary diagnosis of distal radius fractures without expert participation.

Accurate detection of neurofibromas is crucial for quantitative monitoring of tumor progression and surgical assessment. This paper proposes a method for neurofibroma detection in whole-body magnetic resonance imaging (WBMRI) using joint imaging genomics and ensemble learning. Firstly, we enhance texture features through a combination of image sharpening, filtering, brightness adjustment, and contrast enhancement. Then, we employ a weighted boxes fusion (WBF) technique based on test-time augmentation (TTA) under a single model and further integrate multiple models using the dual fusion approach of TTA and WBF. For segmentation, we utilize minimum bounding boxes based on segmentation masks for position calibration. Finally, false positive tumor regions are further eliminated through imaging genomics features. The experimental MRI data is obtained from collaboration between Harvard Medical School and domestic tertiary hospitals, comprising 158 cases with a total of 1380 tumors. Five-fold cross-validation is conducted with segmentation annotations completed by domain experts. Compared to the best results of single models, our proposed method achieves a 10.1% increase in average precision (AP), 7.8% increase in sensitivity, reduction of average false positives to 3.58, a decrease of 17.68, and an 8.5% improvement in competitive performance metric (CPM). This method effectively enhances the accuracy of neurofibroma detection and is applicable to detecting tumors and lesions in other medical imaging applications.

Distal radius fracture (DRF) is one of the most common types of wrist fractures. We aimed to construct a model for the automatic segmentation of wrist radiographs using a deep learning approach and further perform automatic identification and classification of DRF. A total of 2240 participants with anteroposterior wrist radiographs from one hospital between January 2015 and October 2021 were included. The outcomes were automatic segmentation of wrist radiographs, identification of DRF, and classification of DRF (type A, type B, type C). The Unet model and Fast-RCNN model were used for automatic segmentation. The DenseNet121 model and ResNet50 model were applied to DRF identification of DRF. The DenseNet121 model, ResNet50 model, VGG-19 model, and InceptionV3 model were used for DRF classification. The area under the curve (AUC) with 95% confidence interval (CI), accuracy, precision, and F1-score was utilized to assess the effectiveness of the identification and classification models. Of these 2240 participants, 1440 (64.3%) had DRF, of which 701 (48.7%) were type A, 278 (19.3%) were type B, and 461 (32.0%) were type C. Both the Unet model and the Fast-RCNN model showed good segmentation of wrist radiographs. For DRF identification, the AUCs of the DenseNet121 model and the ResNet50 model in the testing set were 0.941 (95%CI: 0.926-0.965) and 0.936 (95%CI: 0.913-0.955), respectively. The AUCs of the DenseNet121 model (testing set) for classification type A, type B, and type C were 0.96, 0.96, and 0.96, respectively. The DenseNet121 model may provide clinicians with a tool for interpreting wrist radiographs.