Aims. Osteoarthritis (OA) is a common degenerative disease that leads to pain, disability, and reduced quality of life. Orientin exhibits considerable anti-inflammatory and antioxidative properties, but its role in chondrocyte senescence and OA progress has not yet been fully characterized. The aim of this study was to evaluate the protective effects of orientin on OA. Methods. The role of orientin in extracellular matrix (ECM) degradation, mitochondrial homeostasis, and chondrocyte senescence was investigated in vitro. Meanwhile, we used molecular docking, small molecular inhibitors, and RNA interference to screen and validate candidate proteins regulated by orientin. In an anterior cruciate ligament transection (ACLT) rat model, radiograph, micro-CT, and various histological examinations were applied to evaluate the therapeutic effects of orientin on OA. Results. We found that orientin inhibited ECM degradation and senescence-associated secretory phenotype (SASP) factor expression in interleukin (IL)-1β-treated chondrocytes. Additionally, orientin reduced the level of reactive oxygen species (ROS) and improved mitochondrial homeostasis. Furthermore, orientin suppressed IL-1β-induced activation of the nuclear factor kappa B (NF-κB) signalling pathway. We also found that orientin bound to phosphoinositide 3-kinase (PI3K) and inhibited NF-κB cascades via the PI3K/AKT pathway. In vivo, we demonstrated that orientin improved cartilage wear and reduced synovial inflammation and osteophyte in an ACLT rat model. Conclusion. Orientin improves mitochondrial homeostasis, inhibits chondrocyte senescence, and alleviates OA progress via the PI3K/AKT/NF-κB axis, which suggests that orientin is a potential effective therapeutic agent for OA. Cite this article: Bone Joint Res 2025;14(3):245–258

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Osteoarthritis (OA) is a widespread chronic degenerative joint disease with an increasing global impact. The pathogenesis of OA involves complex interactions between genetic and environmental factors. Despite this, the specific genetic mechanisms underlying OA remain only partially understood, hindering the development of targeted therapeutic strategies.

Aims. Excessive chondrocyte hypertrophy is a common feature in cartilage degeneration which is susceptible to joint overloading, but the relationship between mechanical overloading and chondrocyte hypertrophy still remains elusive. The aim of our study was to explore the mechanism of mechanical compression-induced chondrocyte hypertrophy. Methods. In this study, the temporomandibular joint (TMJ) degeneration model was built through forced mandibular retrusion (FMR)-induced compression in TMJ. Chondrocytes were also mechanically compressed in vitro. The role of O-GlcNAcylation in mechanical compression-induced chondrocyte hypertrophy manifested through specific activator Thiamet G and inhibitor OSMI-1. Results. Both in vivo and in vitro data revealed that chondrocyte hypertrophic differentiation is promoted by compression. Immunofluorescent and immunoblotting results showed that protein pan-O-GlcNAcylation levels were elevated in these hypertrophic chondrocytes. Pharmacologically inhibiting protein pan-O-GlcNAcylation by OSMI-1 partially mitigated the compression-induced hypertrophic differentiation of chondrocytes. Specifically, runt-related transcription factor 2 (Runx2) and SRY-Box 9 transcription factor (Sox9) were subjected to modification of O-GlcNAcylation under mechanical compression, and pharmacological activation or inhibition of O-GlcNAcylation affected the transcriptional activity of Runx2 but not Sox9. Furthermore, compression-induced protein pan-O-GlcNAcylation in chondrocytes was induced by enhanced expression of glucose transporter 1 (GLUT1), and depletion of GLUT1 by WZB117 dampened the effect of compression on chondrocyte hypertrophy. Conclusion. Our study proposes a novel function of GLUT1-mediated protein O-GlcNAcylation in driving compression-induced hypertrophic differentiation of chondrocytes by O-GlcNAc modification of Runx2, which promoted its transcriptional activity and strengthened the expressions of downstream hypertrophic marker. Cite this article: Bone Joint Res 2025;14(3):209–222

Aims. Diagnostic wrist arthroscopy is considered the gold standard for evaluating wrist joint complaints. Although this tool is often used to diagnose and stage scapholunate ligament (SLL) lesions, reports about the possible findings and their clinical relevance are scarce. Therefore, this study describes the patient characteristics, arthroscopic findings, and treatment of patients who underwent diagnostic arthroscopy for suspected SLL injury. Methods. We conducted a retrospective cohort study of patients who underwent diagnostic wrist arthroscopy due to suspicion of a SLL lesion based on medical history, physical examination, and imaging. We systematically gathered arthroscopic findings and complications. Results. This study included 324 patients, predominantly male (55%), with a median age of 44 years (IQR 29 to 54) and symptom duration of ten months (IQR 5 to 24). The indication of SLL injury was arthroscopically confirmed in 253 patients (78%). Isolated SLL injuries were found in 92 patients (28%) (Geissler I/II: 32%; III: 37%; IV: 32%). SLL lesions and SLL-associated cartilage damage were discovered in 31 patients (10%). Additional findings were found in 181 patients (56%), such as triangular fibrocartilage complex lesions (36%), lunotriquetral ligament lesions (7%), and radioscaphocapitate ligament lesions (11%). No pathology was found in 20 patients (6%). In 27 patients (8%), complications occurred due to wrist arthroscopy. The most common follow-up surgeries were 3LT (40%), salvage procedures (9%), and ulnar shortening osteotomy (6%). Conclusion. While diagnostic wrist arthroscopy commonly confirms the suspected SLL lesions and their severity, it often reveals additional pathologies (un)related to the suspected pathology. It is essential to perform the procedure thoroughly to establish all possible pathologies. Determining the appropriate treatment for these additional findings is not always straightforward and needs further investigation. Cite this article: Bone Jt Open 2025;6(3):312–320

Osteoarthritis (OA) is a highly prevalent and disabling disease with an unmet therapeutic need. The characteristic cartilage loss and alteration of other joint structures result from a complex interaction of multiple risk factors, with mechanical overload consistently playing a central role. This overload generates an inflammatory response in the cartilage due to the activation of the innate immune response in chondrocytes, which occurs through various cellular mechanisms. Moreover, risk factors associated with obesity, being overweight, and metabolic syndrome enhance the inflammatory response both locally and systemically. OA chondrocytes, the only cells present in articular cartilage, are therefore inflamed and initiate an anabolic process in an attempt to repair the damaged tissue, which ultimately results in an aberrant and dysfunctional process. Under these circumstances, where the cartilage continues to be subjected to chronic mechanical stress, proposing a treatment that stimulates the chondrocytes’ anabolic response to restore tissue structure does not appear to be a therapeutic target with a high likelihood of success. In fact, anabolic drugs proposed for the treatment of OA have yet to demonstrate efficacy. By contrast, multiple therapeutic strategies focused on pharmacologically managing the inflammatory component, both at the joint and systemic levels, have shown promise. Therefore, prioritizing the control of chronic innate pro-inflammatory pathways presents the most viable and promising therapeutic strategy for the effective management of OA. As research continues, this approach may offer the best opportunity to alleviate the burden of this incapacitating disease. Cite this article: Bone Joint Res 2025;14(3):199–207

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Paediatric pelvic ring fractures are rare but severe injuries, presenting significant treatment challenges. This study aimed to analyze patient characteristics and explore trends in incidence, treatment methods, and mortality associated with these injuries.

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Nonunion occurs when a fracture fails to heal permanently, often necessitating surgical intervention to stimulate the bone healing response. Current animal models of long-bone nonunion do not adequately replicate human pathological conditions. This study was intended as a preliminary investigation of a novel rat nonunion model using a two-stage surgical intervention, and to evaluate the efficacy of a selective prostaglandin E2 receptor 4 agonist (AKDS001) as a novel nonunion therapeutic agent compared with existing treatments.

The last five years have seen notable advancements in foot and ankle surgery as a result of technical innovations and more consistent reporting of results. Much progress has been made in improving patient-reported outcome measures, in the development of basic research in this area, and in the development of personalized approaches which optimize outcomes for specific groups of patients. This review focuses on five main areas of development within foot and ankle surgery: ankle arthroplasty, osteomyelitis and the diabetic foot, sports injuries, minimally invasive surgery, and orthobiologics. The aim of this annotation is to discuss the progress made in these fields during recent years and propose avenues for further development.

Cite this article: Bone Joint J 2025;107-B(3):283–290.

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The aim of this study was to examine the indications for further surgery and the characteristics of the patients within one year of medial unicompartmental knee arthroplasty (mUKA), providing an assessment of everyday clinical practice and outcomes in a high-volume country.

Aims. A large number of surgical operations are available to treat osteochondral defects of the knee. However, the knee joint arthroplasty materials cannot completely mimic the articular cartilage and subchondral bone, which may bring some obvious side effects. Thus, this study proposed a biocompatible osteochondral repair material prepared from a double-layer scaffold of collagen and nanohydroxyapatite (CHA), consisting of collagen hydrogel as the upper layer of the scaffold, and the composite of CHA as the lower layer of the scaffold. Methods. The CHA scaffold was prepared, and properties including morphology, internal structure, and mechanical strength of the CHA scaffold were measured by scanning electron microscopy (SEM) and a MTS electronic universal testing machine. Then, biocompatibility and repair capability of the CHA scaffold were further evaluated using a rabbit knee cartilage defect model. Results. The CHA scaffold was well suited for the repair of articular cartilage and subchondral bone; the in vitro results showed that the CHA scaffold had good cytocompatibility. In vivo experiments demonstrated that the material had high biocompatibility and effectively induced cartilage and subchondral bone regeneration. Conclusion. The CHA scaffold has a high potential for commercialization and could be used as an effective knee repair material in clinical applications. Cite this article: Bone Joint Res 2025;14(2):155–165

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Our aim was to investigate occurrence of senescent cells directly in tendon tissue biopsies from patients with chronic shoulder tendinopathies, and to correlate senescence with Enhancer of zeste 2 (EZH2) expression, the functional subunit of the epigenetic master regulator polycomb repressive complex.

Aims. To examine how eukaryotic translation initiation factor 5A (eIF5A) regulates osteoarthritis (OA) during mechanical overload and the specific mechanism. Methods. Histological experiments used human bone samples and C57BL/6J mice knee samples. All cell experiments were performed using mice primary chondrocytes. Messenger RNA (mRNA) sequencing was performed on chondrocytes treated with 20% cyclic tensile strain for 24 hours. Western blot (WB) and quantitative polymerase chain reaction were employed to detect relevant indicators of cartilage function in chondrocytes. We created the destabilization of the medial meniscus (DMM) model and the mechanical overload-induced OA model and injected with overexpressing eIF5A adenovirus (eIF5A-ADV). Cartilage degeneration was evaluated using Safranin O/Fast Green staining. Relative protein levels were ascertained by immunohistochemistry (IHC) and immunofluorescence (IF) staining. Results. After OA initiation, eIF5A caused an upregulation of type II collagen (COL2) and a downregulation of matrix metalloproteinase 13 (MMP13), P16, and P21, which postponed the aggravation of OA. Further sequencing and experimental findings revealed that eIF5A knockdown accelerated the progression of OA by boosting the expression of histone acetyltransferase cyclic-adenosine monophosphate response element binding protein (CREB)-binding protein (CREBBP) to mediate activation of the Notch pathway. Conclusion. Our findings identified a crucial functional mechanism for the onset of OA, and suggest that intra-articular eIF5A injections might be a useful therapeutic strategy for OA treatment. Cite this article: Bone Joint Res 2025;14(2):124–135

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Unicompartmental knee arthroplasty (UKA) is associated with an accelerated recovery, improved functional outcomes, and retention of anatomical knee kinematics when compared to manual total knee arthroplasty (mTKA). UKA is not universally employed by all surgeons as there is a higher revision risk when compared to mTKA. Robotic arm-assisted (ra) UKA enables the surgeon to position the prosthesis more accurately when compared to manual UKA, and is associated with improved functional outcomes and a lower early revision risk. Non-randomized data suggests that, when compared to mTKA, raUKA has a clinically meaningful greater functional benefit. This protocol describes a randomized controlled trial that aims to evaluate the clinical and cost-effectiveness of raUKA compared to mTKA for individuals with isolated medial compartment osteoarthritis (OA).

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In our previous research, we have found that melatonin (MEL) affects the osteoporotic process. By balancing bone remoulding, autophagy is involved in age-related bone loss. However, as a regulator of autophagy, whether MEL influences senile osteoporosis via regulating autophagy remains unclear.

The February 2025 Sports Roundup. 360. looks at: Long-term outcomes of focal cartilage lesions of the knee; Comparison of early and delayed multiligament knee reconstruction; Platelet-rich plasma does not improve recovery after partial meniscectomy; Patient height and sex predict semitendinosus autograft diameter

The February 2025 Foot & Ankle Roundup³⁶⁰ looks at:Percutaneous Zadek osteotomy for insertional Achilles tendinopathy; Association of extraosseous arterial diameter with talar dome osteochondral lesions; Autologous chondrocyte implantation for osteochondral lesions of the talus; Symptomatic thromboembolism and mortality in foot and ankle surgery in the UK; Corticosteroid or hyaluronic acid in Morton’s neuroma?

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The Birmingham Orthopaedic Oncology Meeting (BOOM), held in January 2024, convened 309 delegates from 53 countries to discuss and refine 21 consensus statements on the optimal management of chondrosarcoma.

The February 2025 Children’s orthopaedics Roundup³⁶⁰ looks at: Are antibiotics enough for the initial management of paediatric Gustilo-Anderson type I upper limb open fractures?; Advanced imaging for tibial tubercle fractures; Spinal fusion improves quality of life in cerebral palsy scoliosis: a multicentre study; Hip displacement after triradiate closure in ambulatory cerebral palsy; Telehealth validation for adolescent idiopathic scoliosis: comparable clinical measurements enhance access to care; Long-term prognostic markers for residual dysplasia in developmental dysplasia of the hip after closed reduction; Open versus closed reduction for paediatric lateral humeral condyle fractures: better outcomes with closed techniques; Delayed diagnosis of paediatric septic hip leads to poor outcomes and doubling of healthcare costs.