Osteoporosis is a common age-related metabolic bone disease closely associated with osteoblast dysfunction, abnormal apoptosis, and dysregulated autophagy. Naringin, a dihydroflavonoid compound mainly found in citrus fruits and various traditional Chinese medicinal herbs (e.g., Aurantii Fructus Immaturus and Rhizoma Drynariae), exhibits potential anti-aging and osteoprotective effects; however, its specific mechanism requires systematic elucidation. Network pharmacology analysis revealed that the core targets of naringin are significantly enriched in the PI3K/AKT signaling pathway, as well as pathways related to apoptosis and autophagy. Subsequent in vitro experiments demonstrated that naringin promotes osteoblast proliferation, differentiation, and mineralization; upregulates the expression of osteogenic markers; activates protective autophagy; and inhibits apoptosis. By employing the autophagy inhibitor 3-MA and the PI3K/AKT agonist 740Y-P to modulate PI3K/AKT/mTOR-mediated autophagy, we confirmed that the anti-apoptotic effect of naringin is dependent on the activation of autophagy. In vivo, naringin administration inhibited the excessive activation of the PI3K/AKT/mTOR pathway, enhanced autophagy, suppressed excessive apoptosis, ameliorated bone microarchitecture, and increased bone mineral density in ovariectomized mice. Our findings elucidate the mechanism by which naringin exerts its anti-osteoporotic effects through regulating the balance between autophagy and apoptosis, thereby providing a theoretical basis for developing naringin-based anti-aging strategies for bone protection.

Intervertebral disc degeneration (IDD) is a prevalent degenerative disorder and a leading cause of low back pain. Catalpol (CAT) possesses recognized anti-inflammatory and antioxidant properties and shows therapeutic potential for various inflammatory diseases; however, its role in IDD remains unclear. This study aimed to investigate the protective effects of CAT against IDD and to elucidate its underlying mechanism. The study employed both in vitro and in vivo experimental models. The effects of CAT on IDD progression were assessed, with a focus on nucleus pulposus (NP) cell pyroptosis. Mechanistic investigations were conducted to examine the involvement of the NF-κB/NLRP3-mediated pyroptotic pathway, including the nuclear translocation of phosphorylated P65 (p-P65). The dependence of CAT's action on this pathway was further verified through P65 overexpression experiments. CAT was demonstrated to alleviate IDD in experimental models. It exerted its protective effect by inhibiting pyroptosis in NP cells. Mechanistically, CAT blocked the nuclear translocation of p-P65, thereby suppressing the NF-κB/NLRP3-mediated pyroptotic pathway. The reversal of CAT's protective effects upon P65 overexpression confirmed that its action is dependent on this pathway. This study reveals that CAT alleviates IDD by directly targeting P65 to inhibit NP cell pyroptosis via the NF-κB/NLRP3 pathway. These findings identify CAT as a novel therapeutic candidate and provide a mechanistic insight for the treatment of intervertebral disc degeneration.

This study aimed to investigate the anti-osteoporotic mechanisms of naringin in osteoblasts and mice. In vitro, MC3T3-E1 cells were treated with naringin to detect cell proliferation, alkaline phosphatase (ALP) activity, and calcified nodule formation. Western blot was used to analyze the expression of osteogenic markers (OPN, COL1A1, RUNX2) and Wnt/β-catenin pathway proteins (Wnt3a, β-catenin). In vivo, ovariectomized (OVX) mice were treated with naringin for 3 months to observe bone microstructure, femoral histomorphology, and marker expression. Results showed that 0.1, 0.5, and 1 µmol/L naringin significantly promoted cell proliferation, enhanced ALP activity, and increased calcified nodule formation. Naringin also improved bone mineral density (BMD) and trabecular bone number in OVX mice. It elevated serum levels of bone formation markers (P1NP, OCN) while reducing the bone resorption marker CTX-1. Both in vitro and in vivo, naringin upregulated OPN, COL1A1, RUNX2, Wnt3a, and β-catenin expression, and induced β-catenin nuclear translocation. Notably, naringin antagonized the inhibitory effects of XAV939 (a Wnt/β-catenin pathway inhibitor) on OPN, COL1A1, and RUNX2 protein expression. These findings demonstrate that naringin enhances bone density in OVX mice and promotes osteogenic differentiation of MC3T3-E1 cells via activation of the Wnt/β-catenin pathway.

Direct or indirect internal fixation for posterior ankle fractures remains a controversial topic. While direct plate or screw internal fixation is believed to provide better reduction, it may also cause more severe soft tissue damage, while indirect screw internal fixation is thought to result in less damage but may carry the risk of poor reduction. We conducted this meta-analysis to investigate the clinical efficacy and safety of direct versus indirect reduction internal fixation for posterior ankle fractures. The Preferred Reporting Items for Systematic Evaluation and Meta-Analysis (PRISMA) guidelines were used to search the China Knowledge Network database (CNKI), PubMed, Web of Science, Embase, and other databases from the year of establishment- February 2025, and relevant journals were manually searched to collect the relevant literature, and articles that met the requirements were screened and analyzed. Meta-analysis was conducted using RevMan 5.4 software, and a systematic evaluation was carried out when the data from the included studies could not be synthesized. A total of 17 articles involving 1538 study subjects were included, and the results showed that there were no statistical differences in postoperative AOFAS scores, complications, and Dorsiflexion restriction between ankle fractures after direct plate or screw reduction and fixation and those after indirect screw reduction and fixation; however, the Radiological evaluation>2 mm and Osteoarthritis (P < 0.05) were statistically different. Direct reduction and fixation of posterior ankle fractures has better imaging performance and reduces the incidence of postoperative arthritic events.

Glucocorticoid-induced osteoporosis (GIOP) represents the predominant type of secondary bone loss disorder, linked to a substantially elevated incidence of pathological fractures in clinical populations. Modified Yanghe Decoction (MYHD), a classical Chinese medicinal formula, has demonstrated therapeutic potential in managing osteoporotic conditions. Nevertheless, the specific mechanisms underlying MYHD’s effectiveness against GIOP require further elucidation, posing challenges for broader clinical implementation. We performed comprehensive analysis of bioactive constituents in the MYHD n-butanol (MYHD-NB) fraction through high-performance liquid chromatography, followed by mechanistic exploration of its biological effects across experimental models. Ten-week-old male C57BL/6J mice received dexamethasone (DEX)-induced modeling and were administered either MYHD or varying concentrations of MYHD-NB via oral gavage. Following an 8-week intervention, femoral specimens underwent multimodal evaluation including histopathological examination, micro-computed tomography imaging, and advanced molecular detection techniques (immunohistochemistry/immunofluorescence). Parallel bioinformatics analysis was executed on RNA-seq datasets from osteoporotic fracture patients in the GEO repository. For in vitro experimentation, DEX-treated murine BMSCs were employed to assess MYHD-NB’s regulatory effects on cellular proliferation, migratory capacity, osteogenic differentiation potential, and ferroptotic processes. Complementary network pharmacology approaches were utilized to predict potential molecular targets and pathway interactions. MYHD-NB significantly improved the osteoporosis-like phenotype in mice, as indicated by the improvement of bone microstructure and the upregulation of ALP and RUNX2 expression. RNA-seq analysis of the GEO dataset showed that ferroptosis-related genes are significantly upregulated in the femurs of GIOP patients. Both in vivo and in vitro studies confirmed MYHD-NB’s capacity to mitigate dexamethasone-induced ferroptosis in BMSCs while enhancing BMSCs proliferation capacity, migratory potential, and differentiation into osteogenic lineages. Network pharmacology predictions identified HIF-1α as the pivotal regulator mediating MYHD-NB’s anti-ferroptotic effects. Molecular investigations revealed MYHD-NB’s activation of the HIF-1α/GPX4 signaling pathway, with genetic ablation of HIF-1α completely negating the compound’s therapeutic efficacy. MYHD-NB mitigates ferroptosis triggered by DEX in BMSCs while enhancing osteogenic differentiation via the HIF-1α/GPX4 signaling pathway, elucidating its therapeutic mechanism against GIOP. These results demonstrate MYHD-NB’s superior osteogenic potential within the MYHD formulation, positioning it as a promising candidate for alternative GIOP management strategies.

Malignant neoplasm of bone and articular cartilage (MNBAC) represents one of the most prevalent malignant tumours among adolescents. Assessing its disease burden trends is critical for formulating prevention strategies. This study aims to evaluate the temporal trends of MNBAC burden in China, project future trajectories over the next 15 years, and compare these patterns with global benchmarks. Data on incidence, prevalence, deaths, and disability-adjusted life years (DALYs) were extracted from the Global Burden of Disease (GBD) database 2021. Joinpoint regression analysed temporal trends, while decomposition analysis was used to investigate the impact of aging, population growth, and epidemiological factors on the deaths and DALYs rates of MNBAC. Additionally, we conducted BPAC model to project future trends to 2036. Spearman correlation assessed associations between the burden of MNBAC and the socio-demographic Index (SDI). In 2021, China’s age-standardised incidence rate (ASIR), age-standardised prevalence rate (ASPR), age-standardised mortality rate (ASMR) and age-standardised DALYs rate (ASDR) for MNBAC were 1.42, 9.16, 0.93, and 29.52 per 100,000 population, respectively. Compared to 1990, these metrics increased by 118.46

Osteoarthritis (OA) is a chronic inflammatory joint disease associated with aging, trauma, obesity and other pathogenic factors. It is a leading cause of pain and disability worldwide. Macrophages, the most abundant immune cells in the synovium, display significant plasticity and heterogeneity, capable of polarizing into pro-inflammatory M1 or anti-inflammatory M2 types, thus playing a crucial role in the onset and progression of arthritis. Recent studies have increasingly focused on the important role of synovial macrophages in joint homeostasis and suggest that targeting macrophage polarization may emerge as a promising therapeutic strategy for osteoarthritis.

BACKGROUND:Osteoporotic osteoarthritis (OPOA), a distinct subtype of osteoarthritis (OA), has imposed a significant health and economic burden worldwide. However, mechanistic studies and therapeutic strategies for this disease remain in the exploratory stage. PURPOSE:This study aimed to investigate the specific molecular mechanisms by which osteoporosis (OP) exacerbates OA progression through accelerated subchondral bone (SB) sclerosis and the potential of Jiawei Yanghe Decoction (JWYHD) in treating OPOA. METHODS:Key genes in the progression of OPOA were investigated through human clinical sample studies, GEO database analysis, and RNA-seq. The OPOA mouse model was established by a combination of OVX and DMM, with JWYHD administered at different concentrations. In vivo, the pathological status of OPOA and the therapeutic effects of JWYHD were evaluated using behavioral tests, micro-CT, and histopathological examinations. In vitro, the osteogenic differentiation and migration capabilities of mesenchymal stem cells (MSC) were assessed by WB, qRT-PCR, Transwell assays, wound healing assays, and IF co-staining. RESULTS:ITGB6/TGF-β plays a vital role in the pathogenesis of OPOA. A novel concept, the 'Diaphysis-Epiphysis paradox', is hereby proposed, providing a new theoretical framework for research into the pathomechanisms of OPOA from the perspective of abnormal bone mass distribution. By protecting cartilage, regulating the balance of bone mass, and modulating the migration of MSC, JWYHD improves cartilage degeneration and bone mass distribution abnormalities caused by OPOA in an all-around manner. CONCLUSION:Abnormal migration and osteogenic differentiation disorders of MSC accelerate OPOA progression. JWYHD achieved bidirectional regulation of OPOA through ITGB6/TGF-β/β-catenin and CXCL12/CXCR4 multiple signaling pathways.

Osteoarthritis (OA) is the most prevalent degenerative joint disease, characterized by cartilage degradation, chondrocyte apoptosis, synovial inflammation, and subchondral bone remodeling. Accumulating evidence highlights the central role of heat shock proteins (HSPs) in OA pathogenesis and progression. HSPs function as molecular chaperones that maintain proteostasis by facilitating protein folding, preventing aggregation, and modulating stress responses. Dysregulated expression of HSP27, HSP40, HSP60, HSP70, HSP90, and GRP78 contributes to inflammation, extracellular matrix breakdown, and chondrocyte apoptosis, but also provides cytoprotective effects under certain conditions. This duality positions HSPs as both biomarkers of disease activity and promising therapeutic targets. Here, we comprehensively review the roles of HSPs in regulating apoptosis, autophagy, and inflammatory signaling in OA. We further discuss emerging therapeutic strategies that modulate HSP expression or activity, including synthetic drugs, natural products, nanomedicine, stem cell therapy, physical modalities (heat, ultrasound, phototherapy, microwaves), and biological agents such as monoclonal antibodies. By integrating mechanistic insights and translational advances, this review underscores the potential of HSP-targeted therapies to preserve chondrocyte function, maintain extracellular matrix integrity, and slow OA progression, paving the way for novel disease-modifying interventions.

The most appropriate fixation trajectory for posterior malleolar fractures (PMFs) still remains a matter of debate. This meta-analysis aimed to evaluate and compare the outcomes of posteroanterior (PA) and anteroposterior (AP) screw fixation strategies. We conducted a systematic review and meta-analysis following Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. Both manual and electronic searches of multiple databases were conducted. Two independent reviewers screened the studies in accordance with the predefined PICOS criteria: Population (adult patients diagnosed with PMFs); Intervention (PA screw fixation); Comparison (AP screw fixation); Outcome (radiological parameters, screw malpositioning error, American Orthopaedic Foot and Ankle Society (AOFAS) scores, postoperative complications); and Study Design (evidence levels I-III). Statistical synthesis was carried out using Stata 15.1 software (StataCorp LLC, College Station, Texas, USA). A total of 14 articles were included, encompassing 1258 study participants. The findings revealed that there were no statistically significant differences in the postoperative complication rates between the posterior-anterior screw fixation technique and the anterior-posterior screw fixation technique for the management of posterior ankle fractures. Nevertheless, statistically significant differences were observed in the AOFAS scores, the incidence of screw malpositioning, and the radiographic parameters with displacement exceeding 2 mm (P < 0.05). However, the clinical relevance of the difference in AOFAS scores is uncertain. In comparison to the AP method, PA screw fixation yielded superior radiographic outcomes, higher implant accuracy, and better functional recovery as evaluated by the AOFAS scores. The choice of technique should be individualized based on fracture pattern and surgeon expertise.

桡骨远端骨折临床较为常见,好发于老年骨质疏松症患者.有限元分析具有无创、方便、可重复、数据可靠等优点,并能够模拟各种载荷情况,是桡骨远端骨折生物力学研究的首选实验方法.在桡骨远端骨折研究中应用有限元分析,有助于阐明骨折发生机制、评估骨折愈合情况、评估及优化治疗方法.本文对有限元分析在桡骨远端骨折生物力学分析、桡骨远端骨折愈合情况评估及小夹板固定治疗桡骨远端骨折方面的应用进展进行了综述,并对桡骨远端骨折有限元分析的影响因素进行了分析.

目的 研究加味四物汤对全髋关节置换术后贫血及髋关节功能恢复的影响.方法 将60例符合入选标准的患者,按简单随机数字表法分为观察组和对照组,各30例.观察组术后服用加味四物汤,对照组术后服用琥珀酸亚铁片,均连续服用2周.对2组治疗前后的血液相关指标、中医证候积分、视觉模拟量表(VAS)评分、髋关节功能评分(Harris)及疗效进行比较.结果 2组治疗后血红蛋白(Hb)、红细胞比容(HCT)、网织红细胞绝对值均有明显改善,且术后第14天及第30天观察组各指标均优于对照组(P＜0.05).2组VAS评分、Harris评分明显改善,且观察组优于对照组(P＜0.05).观察组贫血疗效总有效率为93.3%(28/30),高于对照组为83.3%(25/30),差异有统计学意义(P＜0.05).观察组中医证候积分总有效率为96.7%(29/30),高于对照组为83.3%(25/30),差异有统计学意义(P＜0.05).结论 加味四物汤对改善全髋关节置换术后患者贫血情况及髋关节功能有着良好的临床效果.

Abstract Background Mendelian randomization analysis was employed to examine the potential causal link between depression and low back pain. This analysis utilizes genetic variants as instrumental variables to help establish a causal relationship. By leveraging the genetic variants associated with depression as the exposure factor, the study aimed to investigate whether there is a causal effect on the development or severity of low back pain. This approach provides valuable insights into the potential causal association between these two conditions. Methods The entire Gene Association Study database (GWAS) was utilized for data mining in a study aiming to investigate the relationship between depression as the exposure factor and low back pain as the outcome factor. Mendelian randomization analysis was performed using regression models such as inverse variance weighting (IVW), the MR‒Egger method, the simple mode method, the weighted median method, and the weighted mode method. The objective was to uncover any potential causal relationship between the exposure factors and the outcome. Results In this study, a total of 25 single nucleotide polymorphism (SNP) loci were utilized as instrumental variables to assess the causal association between depression and low back pain. The inverse variance weighting method estimated that individuals with depression had a 1.71 times higher risk (OR) of experiencing low back pain than the healthy population (95% CI: 1.258 to 2.332, p=0.0006). Similarly, the weighted median method also supported a causal effect between depression and low back pain (95% CI: 1.180 to 2.789, p = 0.0007). Tests for heterogeneity using the inverse variance weighting and MR‒Egger regression methods indicated no significant heterogeneity. Furthermore, the MR‒Egger regression intercept terms and MRPRESSO method tests suggested that the results were less likely to be influenced by genetic pleiotropy. Leave-one-out analyses did not identify any nonspecific SNPs that unduly influenced the results. Overall, these findings provide stronger evidence for a causal relationship between depression and low back pain. Conclusions There may be a positive causal association between depression and low back pain.

目的:探讨肱骨髁上楔形截骨克氏针内固定矫正肱骨髁上骨折并发肘内翻畸形的临床疗效.方法:回顾性分析2014年12月—2019年12月于江西中医药大学附属医院儿童骨科采用肱骨髁上楔形截骨克氏针内固定矫正肱骨髁上骨折并发肘内翻畸形病例24例.测量手术前后提携角及肘关节屈伸活动度,拆除内固定后3个月采用Mayo肘关节功能评分标准评定肘关节功能.结果:24例患儿均获随访,术前提携角为(-15.23±4.21)°,术后提携角为(10.34±3.12)°,平均改变25°,经配对样本t检验,差异有统计学意义(P<0.05);术前肘关节伸直和屈曲活动分别为(-0.35±3.05)°、(112.54±15.78)°,术后肘关节伸直和屈曲活动分别为(0.06±1.02)°、(141.65±7.48)°,肘关节伸直活动差异无统计学意义(P>0.05),肘关节屈曲活动差异具有统计学意义(P<0.05).内固定拆除3个月后,按照Mayo肘关节功能评分标准评定肘关节功能,其中优15例、良6例、中3例.结论:肱骨髁上楔形截骨克氏针内固定是矫正肱骨髁上骨折并发肘内翻畸形的有效方法.

骨伤科手术学是一门理论与实践结合非常紧密的课程,传统教学模式由于缺乏临场性、实践性,已然不能符合现代教育期望.通过分析将虚拟仿真技术运用于骨伤科手术学教学中的应用特点,结合本校教学实践,探索虚拟仿真在未来《骨伤科手术学》领域应用.

Abstract Background: Deep neck space infection is a disease that is often misdiagnosed and may have many rare symptoms. We report a case of upper cervical infection with headache as the primary manifestation and review the relevant literature.Case presentation: A 76-year-old male patient had a recurrent headache for more than one year but was misdiagnosed as cerebrovascular disease. Cervical magnetic resonance imaging showed an abnormal signal of the cervical spine with surrounding tissue edema. A deep neck space infection was diagnosed. We had debridement, and the headache disappeared.Conclusions: This case shows that orthopedics and cardiovascular doctors should improve their understanding of deep neck space infection and avoid misdiagnosis.

目的 观察瘀血痹片治疗胫骨高位截骨术后肿胀的临床效果.方法 回顾性选取2016年7月—2019年5月江西中医药大学附属医院收治的胫骨高位截骨术后肿胀患者50例,根据治疗方法不同分为观察组与对照组各25例.对照组患者给予常规治疗,观察组患者在对照组基础上给予瘀血痹片治疗,2组疗程均为2周.比较2组患者治疗前后膝关节HSS评分、视觉模拟评分法(VAS)评分、焦虑自评量表(SAS)、抑郁自评量表(SDS)评分,治疗后1 d、3 d及5 d的肿胀程度.结果 治疗2周后,2组患者的关节功能、关节活动度、肌肉力量、活动稳定性及屈曲畸形程度评分均高于治疗前,且观察组均高于对照组,差异均有统计学意义(P<0.01);治疗后5 d,观察组患者的肿胀消退程度高于对照组,差异有统计学意义(P<0.05);治疗2周后,2组患者的VAS评分、SAS评分及SDS评分均低于治疗前,且观察组均低于对照组,差异均有统计学意义(P<0.01).结论 瘀血痹片治疗胫骨高位截骨术后肿胀的效果显著,可有效促进膝关节功能恢复,快速减轻肿胀程度,改善疼痛感,缓解患者焦虑、抑郁情绪,值得临床推广应用.

目的 观察加味阳和汤含药血清对MC3T3-E1与RAW264.7细胞共育体系的影响,探究其防治骨质疏松症(OP)肾阳虚证的可能作用机制.方法 制备加味阳和汤含药血清,于Transwell共培养板建立MC3T3-E1与RAW264.7细胞共育体系,设置肾阳虚血清组、空白组、含药血清+肾阳虚血清组及含药血清组.干预48 h后,通过碱性磷酸酶(ALP)和抗酒石酸酸性磷酸酶(TRAP)染色观察成骨、破骨分化;运用TRAP和ALP试剂盒分别检测细胞上清液中TRAP、ALP活性;通过Western blot检测各组OPG、RANKL、RANK蛋白表达.结果 与肾阳虚血清组比较,含药血清+肾阳虚血清组ALP活性增加(P<0.05),TRAP活性及OC数目减低(P<0.05,P<0.05),OPG蛋白表达上调(P<0.05),RANKL、RANK蛋白表达下调(P<0.05,P<0.05).结论 加味阳和汤对OP肾阳虚证有相应治疗作用,其机制可能与增加OPG及降低RANKL、RANK蛋白表达有关.

骨质疏松症(Osteoporosis,OP)是一种常见的全身性代谢性骨疾病,随着中国人口老龄化的加剧,其患病率呈上升趋势.Wnt/β-catenin信号通路对维持机体骨重建的动态平衡发挥着重要作用,目前被广泛用于OP的研究.大量分子生物学实验表明,中药单体及中药复方可通过调节Wnt/β-catenin信号通路,影响成骨细胞和骨髓间充质干细胞的增殖、分化及活性等,增加骨形成,从而发挥治疗OP的作用.综述近年来中药单体与中药复方经Wnt/β-catenin信号通路治疗OP的相关研究成果,以期为中药研发及临床防治提供思路.