Bone regeneration faces many critical challenges in clinical settings, particularly concerning repairing materials, such as source shortage, insufficient osteoinductive activity and surgical complexity. Herein, the mineralizable and injectable biomimetic collagen hydrogel (MH) was developed for fabricating bone tissue. Through the MH system, the collagen-binding-domain fused bone morphogenetic protein-2 (CBD-BMP-2) could be controllably released; the rat bone mesenchymal stem cells (BMSCs) were induced to in vitro form bone-like tissue as micro computed tomography (micro-CT) scanning; the rat back subcutaneous injection experiments demonstrated cells could be in situ recruited to engineer bone-like tissue reaching 6.53 f 3.45 MPa of compression modulus; in the rat calvarial bone-defect model, minimally invasive surgery (MIS) could be easily operated and in situ regenerate calvarial bone, showing 1.44 f 0.05 g/cm3of Bone Mineral Density (BMD), 60.62 f 4.30 % of Bone Volume/ Total Volume (BV/TV), 1.95 f 0.02 mm-1 of Trabecular Number (Tb.N) and 0.30 f 0.03 mm of Trabecular Thickness (Tb.Th), similar to normal calvarial bone. Our study indicates that the MH-based bone regenerative system has the potential to promote bone formation and offers a promising solution in orthopedic application.

Osteoarthritis (OA) is characterized by sterile intra-articular inflammation and progressive cartilage degeneration. Nanoparticle-based photothermal therapy (PTT) offers a promising intervention for OA therapy; however, drug-release control under photothermal conditions remains underexplored. Here, we present a Prussian blue-based, near-infrared (NIR) -responsive hydrogel (GPT) that enables multi-target therapy for OA through co-encapsulation of Prussian blue nanoparticles (PBNPs) and tannic acid (TA) within a thermosensitive agarose matrix. TA coordinates with unsaturated iron sites on PBNPs, synergistically enhancing antioxidant capacity while maintaining robust photothermal performance. Harnessing the thermal phase transition of low-melting-point agarose, GPT enables precise, temperature-dependent drug release: NIR irradiation triggers accelerated release within a mild therapeutic window, whereas drug release slowly in the absence of stimulation. Co-released TA/PBNPs rapidly scavenge excessive reactive oxygen species (ROS), delay chondrocyte senescence, and restore metabolic homeostasis. Moreover, the localized hyperthermia activates HSP70, enhancing chondroprotection under inflammatory stress. In mice model of OA, GPT/NIR treatment effectively slows disease progression. Transcriptomic profiling further reveals suppression of IL-17 signaling as a key mechanism contributing to reduced cartilage degradation. This platform synergistically combines controlled drug delivery and PTT, achieving unprecedented integration of IL-17 pathway inhibition with a photothermal-antioxidant system for OA treatment. It enables concurrent metabolic reprogramming and structural preservation, offering a novel strategy for disease-modifying OA therapy.

Shuo Qiang,1 Yunke Liu,1 Yonghui Dong,1 Cheng Cheng,1 Yifan Huang,1 Jia Zheng,1 Chao Tang,1 Siyu Zhao21Department of Orthopedics, Zhengzhou University People’s Hospital, Zhengzhou, Henan, People’s Republic of China; 2Department of Intensive Care Unit, The First Affiliated Hospital of Jinan University, Jinan, Guangdong, People’s Republic of ChinaCorrespondence: Siyu Zhao, Email zsyguke@163.com Chao Tang, Email 56091352@qq.comBackground: FibroNPC is a degeneration associated subtype in intervertebral disc degeneration (IVDD), yet its markers and immune crosstalk remain poorly characterized. ITGBL1 and RPN1 recur as IVDD associated genes in bulk studies, but where they are expressed within the heterogeneous disc has not been resolved.Methods: Three GEO datasets comprising 81 bulk profiles were integrated and screened by LASSO, SVM-RFE, and Random Forest, with external validation in an independent 15 sample cohort. Two human IVDD scRNA-seq cohorts were analyzed by subclustering, signature scoring, and within scRNA-seq per-subpopulation contribution analysis. CellChat, AUCell pathway scoring, and drug prediction were used as exploratory analyses; IL-1β stimulated HNPCs served as the in vitro model.Results: Machine learning analysis prioritized ITGBL1 and RPN1 as consensus core genes (combined AUC = 0.925), with their differential expression further supported in an independent external cohort. Single cell mapping preferentially localized both genes to a FibroNPC subpopulation and associated this cell state with coupled integrin/focal adhesion and ER protein processing/N-glycosylation programs. Notably, although FibroNPCs comprised less than one-fifth of NP/AF cells, they contributed approximately 48% of total ITGBL1 expression and disproportionate shares of several canonical fibrotic transcripts. CellChat further inferred increased macrophage SPP1–integrin communication involving structural cell populations in IVDD. In IL-1β stimulated HNPCs, both ITGBL1 and RPN1 were increased at the mRNA and protein levels.Conclusion: ITGBL1 and RPN1 represent FibroNPC associated molecular markers linked to coupled integrin signaling and N-glycosylation programs in IVDD. The disproportionate contribution of FibroNPCs to ITGBL1 and fibrotic gene expression highlights the importance of cell state resolved localization beyond conventional bulk hub-gene identification. Further functional validation is required before therapeutic implications can be established.Keywords: IVDD, single-cell RNA sequencing, ITGBL1, RPN1, FibroNPC, pseudotime

Impaired macrophage polarization is a key factor exacerbating osteoporosis (OP), influencing bone metabolism via modulating the osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs). Histone cell cycle regulator (HIRA), an epigenetic regulator, is downregulated in OP. However, its role in modulating macrophage polarization and BMSCs osteogenic differentiation remains unclear. Bone marrow-derived macrophages (BMDMs) and BMSCs were extracted from the bone marrow of SD rats, and identified using staining and flow cytometry. An ovariectomized (OVX) mouse model was established, and HIRA protein was detected via Western blot. A co-culture system of BMDMs and BMSCs was established, and BMDMs were transfected with an HIRA overexpression plasmid. Cytokine levels were measured by ELISA kits, bone structure was assessed via micro-CT, and histopathological staining evaluated femoral tissue pathology, calcium deposition, and osteoclast counts. The levels of proteins associated with osteogenic differentiation, osteoclast differentiation, macrophage polarization, and the YAP1/β-catenin pathway were detected using Western blot. HIRA is downregulated in BMSCs treated with dexamethasone and in the femoral tissues of OVX mice. Overexpression of HIRA effectively raised M2 polarization markers and reduced M1 polarization markers in BMDMs, and promoted BMSCs osteogenic differentiation. Following HIRA overexpression in OVX mice, femoral tissue damage was significantly reduced, osteoclast numbers decreased, and bone metabolic imbalance improved. Furthermore, HIRA overexpression also activated the YAP1/β-catenin axis in the femoral tissue of OVX mice, thereby suppressing bone loss and promoting macrophage M2 polarization. HIRA promotes M2 polarization of macrophages by activating the YAP1/β-catenin pathway, thereby enhancing BMSC osteogenic differentiation and ultimately reducing bone loss in OVX mice. Overexpression of histone cell cycle regulator (HIRA) promotes M2 polarization of BMDMs by activating the YAP1/β-catenin pathway, thereby promoting BMSCs osteogenic differentiation and declining bone loss in OVX mice.

[This corrects the article DOI: 10.3389/fcell.2022.820922.].

Objective: More and more evidence show that diabetes is closely related to osteoarthritis (OA). However, the role and mechanism of DNA damage-inducible transcript 4 protein (DDIT4) in diabetic OA (DOA) have not been clarified. Methods: We collected OA patients and non-OA subjects who underwent total knee replacement surgery, and analyzed the DDIT4 expression in synovial samples using RT-qPCR. The cell viability of fibroblast-like synoviocytes (FLSs) was measured by CCK-8 assay. Annexin V-FITC/PI double staining was used to detect the cell apoptosis. Scratch and Transwell assays were used to determine cell migration and invasion, respectively. Results: The levels of cellular inflammatory factors (IL-1β, IL-6 and TNF-α), oxidative stress and glycolysis related indicators were detected by using kits. Western blot was used to determine the expression of DDIT4, Aggrecan, COL3A1, MMP3, MMP13, HK2, PFKP and PKM2 in FLSs or ATDC5 cells. The results showed that the expression level of DDIT4 was significantly reduced in the synovial samples of OA patients and primary FLSs. Functional studies showed that DDIT4 overexpression inhibited the overactivation, migration, and invasion of FLSs, as well as alleviated chondrocyte injury co-cultured with FLSs. Importantly, the expression of DDIT4 was down-regulated in patients with DOA and closely related to DOA. Further research found that high glucose (HG) promoted excessive activation, migration, and invasion of FLSs, and exacerbated the followed chondrocyte injury. Overexpression of DDIT4 alleviated HG-induced abnormal function of FLSs and injury to chondrocytes. Importantly, DDIT4 inhibited lactate synthesis, glucose uptake, LDH activity, extracellular acidification rate, oxygen consumption rate, and expression levels of glycolysis related protein (HK2, PFKP, PKM2) in HG-induced FLSs. And the glycolysis inhibitors (Cyto-B and 3BrPA) alleviated the injury of ATDC5 chondrocytes co-cultured with FLSs. Conclusions: DDIT4 participates in HG-induced FLSs overactivation and inflammation response, as well as chondrocyte injury and OA progression by regulating glycolysis processes.

Aseptic loosening (AL) of artificial hip joints is the most common complication following hip replacement surgery. A total of eight patients diagnosed with AL following total hip arthroplasty (THA) undergoing total hip replacement and eight control patients diagnosed with avascular necrosis of femoral head (ANFH) or femoral neck fracture undergoing THA were enrolled. The samples of the AL group were from synovial tissue surrounding the lining/head/neck of the prosthesis, and the samples of the control group were from the synovium in the joint cavity. The present study utilized second‑generation high‑throughput sequencing and mass spectrometry to detect differentially expressed genes, proteins and metabolites in the samples, as well as Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analysis. Key genes cytokine receptor‑like factor‑1 (CRLF1) and glutathione‑S transferase µ1 (GSTM1) expression levels were verified by reverse transcription‑quantitative PCR and western blotting. The integrated transcriptomics, proteomics and untargeted metabolomics analyses revealed characteristic metabolite changes (biosynthesis of guanine, L‑glycine and adenosine) and decreased CRLF1 and GSTM1 in AL, which were primarily associated with amino acid metabolism and lipid metabolism. In summary, the present study may uncover the underlying mechanisms of AL pathology and provide stable and accurate biomarkers for early warning and diagnosis.

Background:Aseptic loosening (AL) of hip prostheses is one of the main reasons for revision total hip arthroplasty (rTHA). However, the transcriptomic characteristics of AL are scarcely understood. This study aimed to discover candidate biomarkers for the diagnosis of AL. Patients and methods:The interface membrane from four patients with AL of hip prostheses and the synovium samples from four patients with a periprosthetic femoral fracture (PFF) after total hip arthroplasty (THA) were analyzed via RNA sequencing. Integrated bioinformatics analysis was employed to identify immune-related hub genes in AL. Immune cell infiltration analysis and correlation analysis were performed. Connectivity map analysis was utilized to predict the potential small-molecule compounds for AL treatment. Western blotting and histological staining were used to verify the expression of hub genes in AL. Results:A total of 2,184 differentially expressed genes (DEGs) were identified in the AL samples, including 2,050 upregulated genes and 134 downregulated genes, and these DEGs were mainly enriched in immune cell-related signaling pathways and immune-related processes. Immune cell infiltration analysis showed that the proportion of M1 macrophages increased in AL. Three genes closely related to M1 macrophages were screened, namely, CD68, CD163, and SPP1, according to the results of correlation analysis. Hematoxylin-eosin staining showed that the synovitis score of AL samples was significantly higher than that of controls (average, 6.2 vs. 3.8). Western blotting and immunohistochemical analysis showed that the expression of CD68, CD163, and SPP1 in the AL group was significantly higher than that in the control group. The top 10 compounds with the highest negative scores were predicted to be potential therapeutic drugs for the treatment of AL. Conclusion:Preliminary transcriptomic signatures suggested that CD68, CD163, and SPP1 may serve as potential biomarkers for AL, offering a novel research perspective for future diagnosis and therapeutic intervention of AL.

Osteoarthritis (OA) is a complex, progressive, and age-associated disease characterized by aberrant epigenetic expression. Epigenetic analysis has helped clarify the role of histone post-translational modifications (PTMs) in OA. PTMs affect histone structure and function and, therefore, regulate the expression of genes implicated in various biological processes. The roles of histone methylation and acetylation in OA progression-including extracellular collagen degradation and matrix destruction-have been thoroughly analyzed. Though several studies have shown that histone PTMs are related to OA, summative investigations in this area are lacking. The present literature review examines the relationships between histone PTMs and OA. It focuses mainly on methylation, acetylation, phosphorylation, lactylation, ubiquitination, and the roles of the histone methyltransferase (HMT)/histone demethylase (HDMT) and histone acetyltransferase (HAT)/histone deacetylase (HDAC) families in OA development. We used epigenetic tools for discovering new OA treatments. This review offers new perspectives for future studies on OA pathogenesis and treatment.

Cellular senescence was implicated in the pathogenesis of age-related diseases such as osteoarthritis (OA). Increasing evidence suggests that alterations in the OA joint microenvironment play a crucial role in the pathogenesis of OA. This study aims to establish a clear link between the impact of accumulated lactate on the senescence of fibroblast-like synoviocytes (FLS) within the OA microenvironment. OA models and models with intra-articular injection of lactate were established in rat models, histological analyses were performed. Human OA-FLS treated with lactate was analyzed by mRNA sequencing, senescence related experiments and underlying signaling pathway activation were comprehensively evaluated. This study confirmed that OA models and lactate-injection models exhibited higher synovitis scores. Enrichment analyses indicated dysregulated cell cycle and cellular senescence pathways in OA-FLS treated with lactate. Lactate significantly up-regulated arginase 2 (ARG2) expression and promoted OA-FLS senescence, including G1/S arrest, increased reactive oxygen species and β-galactosidase production, high expression of senescence-associated secretory phenotype factors, which could be attenuated by siRNA-Arg2. The ARG2-mTOR/S6K1 axis was identified as a potential signaling for lactate-induced OA-FLS senescence, and activated mTOR/S6K1 signaling could be reduced by siRNA-Arg2, rapamycin (mTOR inhibitor), and LY294002 (PI3K inhibitor). Our study provides novel targets and insights for OA therapies.

Background Interactions between the immune and metabolic systems may play a crucial role in the pathogenesis of metabolic syndrome-associated rheumatoid arthritis (MetS-RA). The purpose of this study was to discover candidate biomarkers for the diagnosis of RA patients who also had MetS.Methods Three RA datasets and one MetS dataset were obtained from the Gene Expression Omnibus (GEO) database. Differential expression analysis, weighted gene co-expression network analysis (WGCNA), and machine learning algorithms including Least Absolute Shrinkage and Selection Operator (LASSO) regression and Random Forest (RF) were employed to identify hub genes in MetS-RA. Enrichment analysis was used to explore underlying common pathways between MetS and RA. Receiver operating characteristic curves were applied to assess the diagnostic performance of nomogram constructed based on hub genes. Protein-protein interaction, Connectivity Map (CMap) analyses, and molecular docking were utilized to predict the potential small molecule compounds for MetS-RA treatment. qRT-PCR was used to verify the expression of hub genes in fibroblast-like synoviocytes (FLS) of MetS-RA. The effects of small molecule compounds on the function of RA-FLS were evaluated by wound-healing assays and angiogenesis experiments. The CIBERSORT algorithm was used to explore immune cell infiltration in MetS and RA.Results MetS-RA key genes were mainly enriched in immune cell-related signaling pathways and immune-related processes. Two hub genes (TYK2 and TRAF2) were selected as candidate biomarkers for developing nomogram with ideal diagnostic performance through machine learning and proved to have a high diagnostic value (area under the curve, TYK2, 0.92; TRAF2, 0.90). qRT-PCR results showed that the expression of TYK2 and TRAF2 in MetS-RA-FLS was significantly higher than that in non-MetS-RA-FLS (nMetS-RA-FLS). The combination of CMap analysis and molecular docking predicted camptothecin (CPT) as a potential drug for MetS-RA treatment. In vitro validation, CPT was observed to suppress the cell migration capacity and angiogenesis capacity of MetS-RA-FLS. Immune cell infiltration results revealed immune dysregulation in MetS and RA.Conclusion Two hub genes were identified in MetS-RA, a nomogram for the diagnosis of RA and MetS was established based on them, and a potential therapeutic small molecule compound for MetS-RA was predicted, which offered a novel research perspective for future serum-based diagnosis and therapeutic intervention of MetS-RA.

Osteoarthritis (OA) is a progressive degenerative disease resulting in joint deterioration. It is a whole organ disease characterized by cartilage degeneration and varying degrees of synovitis, involving pathological changes in all joint tissues, such as cartilage, subchondral bone, ligaments, meniscus, synovium, and infrapatellar fat pad (IPFP). IPFP is the largest adipose tissue structure in the knee joint and is composed of fat cells, immune cells and blood vessels. Moreover, IPFP is located close to the cartilage and bone surface so that it may reduce the impact of loading and absorb forces generated through the knee joint, and may have a protective role in joint health. IPFP has been shown to release various cytokines and adipokines that play pro-inflammatory and pro-catabolic roles in cartilage, promoting OA progression. Intra-articular injections of IPFP-derived mesenchymal stem cells and exosomes have been shown to reduce pain and prevent OA progression in patients with knee OA. Previous studies have shown that IPFP has a biphasic effect on OA progression. This article reviews the latest research progress of IPFP, discusses the role and mechanism of IPFP in OA, provide new intervention strategies for the treatment of OA. This article will also discuss the handling of IPFP during the procedure of total knee arthroplasty.

Infective bone defect is increasingly threatening human health. How to achieve the optimal antibacterial activity and regenerative repair of infective bone defect simultaneously is a huge challenge in clinic. Herein, this work reports a rational integration of Mn single-atom nanozyme into the 3D-printed bioceramic scaffolds (Mn/HSAE@BCP scaffolds). The integrated Mn/HSAE@BCP scaffolds can catalyze the conversion of H2O2 to produce hydroxyl radical (•OH) and superoxide anion (O2 •-) through cascade reaction. Besides, the prominent thermal conversion efficiency of Mn/HSAE@BCP scaffolds can be utilized for sonodynamic therapy (SDT). The synergetic strategy of chemodynamic therapy (CDT)/SDT enables the sufficient generation of reactive oxygen species (ROS) to kill Staphylococcus aureus (S. aureus) or Escherichia coli (E. coli). Furthermore, the enhanced antibacterial efficacy of Mn/HSAE@BCP scaffolds is beneficial to upregulate the expression of osteogenesis-related markers (such as collagen 1(COL1), Runt-related transcription factor 2 (Runx2), osteocalcin (OCN), and osteoprotegerin (OPG)) in vitro and further promote bone regeneration in vivo. The results demonstrate the good potential of Mn/HSAE@BCP scaffolds for the enhanced antibacterial activity and bone regeneration, which provide an effective method for the treatment of clinical infective bone defect.

In previous reports, hypothyroidism, hypopituitrism, and hypogonadism were common endocrine causes of SCFE, but this is the first time that congenital adrenal hyperplasia has been observed. As such, patients who have undergone long-term endocrine treatment for congenital adrenal hyperplasia could potentially be subjected to a higher risk for SCFE.

Background: Slipped capital femoral epiphysis (SCFE) is a common hip problem in adolescents between the ages of 8 and 15. Various endocrine disorders have been reported as the cause of this condition. Here, we describe a rare case of a boy with SCFE secondary to congenital adrenal hyperplasia (CAH). Case presentation: We report a 12-year-old boy who was admitted to our hospital for right SCFE that was not caused by trauma. The patient was diagnosed with CAH two months after birth and subsequently started long-term treatment with hydrocortisone and 9α-fludrocortisone. From the age of 5, he was treated with growth hormone and gonadotropin-releasing hormone (GnRH) analogs to improve height. After adequate endocrine evaluation and endocrine therapy, the patient underwent surgery for right SCFE. Conclusion: In previous reports, hypothyroidism, hypopituitarism, and hypogonadism were common endocrine causes of SCFE, but this is the first time that congenital adrenal hyperplasia has been observed. As such, patients who have undergone long-term endocrine treatment for congenital adrenal hyperplasia could potentially be subjected to higher risk for SCFE.

目的 观察原发性膝骨关节炎患者行后稳定型全膝关节置换术前、后胫骨平台后倾角(posterior tibial slope,PTS)变化,探讨其对术后膝关节功能的影响.方法 219例原发性膝骨关节炎患者均行单侧初次后稳定型全膝关节置换术,分别于术前2 d、术后12个月行站立位膝关节侧位X线检查,测量PTS,计算手术前后PTS差值(△PTS).219例患者根据△PTS均值(5.13°)分为小△PTS组87例(△PTS≤5.13°)和大△PTS组132例(△PTS＞5.13°),比较2组术前2 d、术后12个月膝关节活动范围(range of motion,ROM)、疼痛视觉模拟评分(visual analogue scale,VAS)、西安大略和麦克马斯特大学骨关节炎评分(the Western Ontario and McMaster Universities Osteoarthritis index,WOMAC)、美国膝关节协会评分(American Knee Society score,KSS).采用Pearson相关法分析行后稳定型全膝关节置换术的原发性膝骨关节炎患者△PTS与术后ROM、VAS评分、WOMAC评分、KSS评分的相关性.结果 小△PTS组术前ROM[(105.64±15.32)°]及 VAS 评分[(5.89±1.47)分]、WOMAC 评分[(101.74±11.34)分]、KSS 临床评分[(43.75± 16.31)分]、KSS 功能评分[(41.10±15.24)分]与大△PTS 组[(106.17±16.52)°、(6.12±1.24)分、(106.39±9.28)分、(41.42±17.61)分、(39.62±14.31)分]比较差异均无统计学意义(P＞0.05);术后小△PTS组、大△PTS组ROM[(121.64±11.34)°、(116.12±12.69)°]及 KSS 临床评分[(82.18±9.12)、(80.42±10.63)分]、KSS 功能评分[(80.13±7.11)、(77.41±6.39)分]均高于术前(P＜0.05),VAS 评分[(1.73±1.22)、(1.66±1.41)分]、WOMAC 评分[(38.86±6.94)、(42.18±7.18)分]均低于术前(P＜0.05);小 △PTS 组术后 ROM 大于大 △PTS 组(t=1.793,P=0.017),术后VAS评分、WOMAC评分、KSS临床评分、KSS功能评分与大△PTS组比较差异均无统计学意义(P＞0.05).行后稳定型全膝关节置换术的原发性膝骨关节炎患者△PTS与术后ROM呈负相关(r=-0.634,P=0.028),与术后VAS评分、WOMAC评分、KSS临床评分、KSS功能评分均无相关性(P＞0.05).结论 原发性膝骨关节炎患者行后稳定型全膝关节置换术后PTS变化较小者ROM增大,△PTS≤5.13.可提高术后膝关节屈曲度,改善患者膝关节功能.

Isobavachalcone (IBC), an active component isolated from Psoralea corylifolia L., has been used extensively to treat a wide range of inflammation-associated diseases. However, little is known regarding the potential effect of IBC in the treatment of osteoarthritis (OA). The purpose of this research was to investigate the potential therapeutic effectsof IBC on OA by performingin vitroand in vivo experiments. Meanwhile, the underlying mechanism responsibles for that effect was also explored. Primary rat chondrocytes were isolated from the knee cartilage, and then pretreated with various concentrations of IBC followed by stimulation with or without LPS (1 µg/ml) for the indicated times. In vitro, the expression levels of iNOS, COX-2, MMP3, MMP13, ADAMTS5, aggrecan, and collagen II were determined by qRT-PCR, western blot, and immunofluorescence staining. In addition, western blot analysis and immunofluorescence were used to assess alterations to the NF-κB signaling pathway. In vivo, an ACLT-induced rat OA model was established in order to determine the protective effect of IBC. The results showed that IBC treatment inhibited the upregulation of inflammatory factors such as iNOS and COX-2 in response to LPS stimulation. Moreover, IBC significantly suppressed the expression of MMP-3, MMP-13, and ADAMTS5 induced by LPS in a dose-dependent manner. Furthermore, the LPS-induced reduction of collagen II and aggrecan was reversed by IBC. Mechanistically, IBC significantly decreased LPS-induced p65 phosphorylation and IκBα degradation as well as suppressed nuclear translocation of p65 in rat chondrocytes as evidenced by western blot analysis and immunofluorescence staining, indicating that IBC effectively inhibited the LPS-induced activation of the NF-κB pathway. In vivo, IBC treatment prevented cartilage degeneration in the ACLT-induced rat model. In summary, our results suggest that IBC may be able to act as a promising therapeutic drug for treating OA.

目的 观察联合应用胫骨高位截骨手术和膝关节镜下的骨髓刺激手术处理膝内侧单间室骨关节炎的临床效果.方法 从2018年1月至2019年4月期间,选择21例在商丘市第一人民医院治疗的膝内侧单间室病变的骨关节炎患者,均采用了联合应用胫骨高位截骨术和关节镜下手术治疗,采用疼痛视觉模拟评分(visual ana-logue scale,VAS),Lysholm评分量表,美国膝关节协会评分(American knee society knee Score,AKS)进行评价,通过影像学进行评价,在负重位下肢全长X线上观察胫骨近端内侧角(medial proximal tibial angle,MPTA),在膝关节磁共振上对软骨进行Noyes评分.观察术后并发症发生情况.结果 为期2年的随访,21例患者术后均未出现并发症.术后的疼痛VAS评分较术前明显降低,差异存在统计学意义(P＜0.05).Lysholm评分、AKS评分,术前和术后比较,评分改善,具有统计学意义(P＜0.05).MPTA角,术前和术后2周对比,角度明显改善,存在统计学意义(P＜0.05).Noyes评分分级,术前和术后半年比较,分级下降,存在统计学意义(P＜0.05).结论 联合应用胫骨高位截骨手术和关节镜下骨髓刺激手术治疗,可以改善骨关节炎患者的关节力线,改善关节功能,为内侧软骨再生创造良好的环境,能较快缓解术前疼痛,并能保持治疗效果.

[目的]探讨抗生素骨水泥间置治疗假体周围感染(periprosthetic joint infection,PJI)失败的危险因素.[方法]回顾性分析本院2017年1月—2020年7月收治的69例PJI患者的临床资料.根据患者抗生素骨水泥间置术后是否出现再次感染,将其分为再感染组和治愈组.采用单因素比较和Cox分析探讨抗生素骨水泥间置术后再次感染的影响因素.[结果]所有患者均获随访,随访时间0.5～52.9个月,69例患者中,15例抗生素骨水泥间置术后出现了再次感染的情况,感染发生时间为术后0.5～9.1个月,中位感染发生时间为术后2.2个月.单因素比较表明,两组患者在年龄、性别构成、吸烟史、饮酒史、ASA等级、aCCI评分、糖尿病、高血压、冠心病、类风湿性关节炎、既往感染史及微生物学培养结果的差异均无统计学意义(P＞0.05);但是,再感染组的既往髋膝关节翻修史比率[是/否,(5/10)vs(4/50),P＜0.05]和窦道比率[是/否,(7/8)vs(9/45),P＜0.05]显著高于治愈组.Cox 分析表明,既往髋膝关节翻修(HR=3.755,95％CI 1.264～11.152,P=0.017)及存在窦道(HR=2.834,95％CI 1.018～7.885,P=0.046)是PJI患者经抗生素骨水泥间置术后再发感染的独立危险因素.[结论]既往髋膝关节翻修史及存在窦道是PJI患者经抗生素骨水泥间置术后再发感染的独立危险因素,应引起临床医生重视.

Objective: To investigate the rate of periprosthetic joint infection (PJI) revision surgeries and clinical information of hip-/knee- PJI cases nationwide from 2015 to 2017 in China. Methods: An epidemiological investigation. A self-designed questionnaire and convenience sampling were used to survey 41 regional joint replacement centers nationwide from November 2018 to December 2019 in China. The PJI was diagnosed according to the Musculoskeletal Infection Association criteria. Data of PJI patients were obtained by searching the inpatient database of each hospital. Questionnaire entries were extracted from the clinical records by specialist. Then the differences in rate of PJI revision surgery between hip- and knee- PJI revision cases were calculated and compared. Results: Total of 36 hospitals (87.8%) nationwide reported data on 99 791 hip and knee arthroplasties performed from 2015 to 2017, with 946 revisions due to PJI (0.96%). The overall hip-PJI revision rate was 0.99% (481/48 574), and it was 0.97% (135/13 963), 0.97% (153/15 730) and 1.07% (193/17 881) in of 2015, 2016, 2017, respectively. The overall knee-PJI revision rate was 0.91% (465/51 271), and it was 0.90% (131/14 650), 0.88% (155/17 693) and 0.94% (179/18 982) in 2015, 2016, 2017, respectively. Heilongjiang (2.2%, 40/1 805), Fujian (2.2%, 45/2 017), Jiangsu (2.1%, 85/3 899), Gansu (2.1%, 29/1 377), Chongqing (1.8%, 64/3 523) reported relatively high revision rates. Conclusions: The overall PJI revision rate in 34 hospitals nationwide from 2015 to 2017 is 0.96%. The hip-PJI revision rate is slightly higher than that in the knee-PJI. There are differences in revision rates among hospitals in different regions.