Journal of Orthopaedic Translation最新文献

{"title":"Current status of nano-embedded growth factors and stem cells delivery to bone for targeted repair and regeneration","authors":"Wenqing Liang , Chao Zhou , Xiankun Liu , Qiong Xie , Linying Xia , Lu Liu , Wenwen Bao , Hongming Lin , Xiaochun Xiong , Hao Zhang , Zeping Zheng , Jiayi Zhao","doi":"10.1016/j.jot.2024.12.006","DOIUrl":"10.1016/j.jot.2024.12.006","url":null,"abstract":"<div><div>Bone-related diseases like osteoarthritis and osteoporosis impact millions globally, affecting quality of life. Osteoporosis considerably enhances the probability of bone fractures of the wrist, hip, and spine. Enhancement and acceleration of functional bone development can be achieved through the sustained delivery of growth factors (GFs) and cells in biomaterial carriers. The delivery of bioactive compounds in a targeted, spatiotemporal way that most closely resembles the natural defect repair process can be achieved by designing the carrier system with established release kinetics. Furthermore, the carrier can serve as a substrate that mimics the extracellular matrix, facilitating osteoprogenitor cell infiltration and growth for integrative tissue healing. In this report, we explore the significance of GFs within the realm of bone and cartilage tissue engineering, encompassing their encapsulation and delivery methodologies, the kinetics of release, and their amalgamation with biomaterials and stem cells (SCs) to facilitate the mending of bone fractures. Moreover, the significance of GFs in evaluating the microenvironment of bone tissue through reciprocal signaling with cells and biomaterial scaffolds is emphasized which will serve as the foundation for prospective advances in bone and cartilage tissue engineering as well as therapeutic equipment. Nanoparticles are being used in regenerative medicine to promote bone regeneration and repair by delivering osteoinductive growth factors like BMP-2, VEGF, TGF-β. These nanocarriers allow controlled release, minimizing adverse effects and ensuring growth factors are concentrated at the injury site. They are also mixed with mesenchymal stem cells (MSCs) to improve their engraftment, differentiation, and survival. This approach is a key step in developing multi-model systems that more efficiently facilitate bone regeneration. Researchers are exploring smart nanoparticles with immunomodulatory qualities to improve bonre regeneration and reduce inflammation in injury site. Despite promising preclinical results, challenges include cost management, regulatory approval, and long term safety. However, incorporating stem cell transport and growth factors in nanoparticles could revolutionize bone regeneration and offer more personalized therapies for complex bone disorders and accidents.</div></div><div><h3>The translational potential of this article</h3><div>Stem cell transport and growth factors encapsulated in nanoparticles are becoming revolutionary methods for bone regeneration and repair. By encouraging stem cells to develop into osteoblasts, osteoinductive GFs like BMP-2, VEGF, and TGF-β can be delivered under control due to nanomaterials like nanoparticles, nanofibers, and nanotubes. By ensuring sustained release, these nanocarriers lessen adverse effects and enhance therapeutic results. In order to prove their survival and development, MCSs, which are essential for bone regeneration, are mixe","PeriodicalId":16636,"journal":{"name":"Journal of Orthopaedic Translation","volume":"50 ","pages":"Pages 257-273"},"PeriodicalIF":5.9,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11788687/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143122818","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Moderate static magnetic field regulates iron metabolism and salvage bone loss caused by iron accumulation","authors":"Chenxiao Zhen , Shenghang Wang , Jiancheng Yang , Gejing Zhang , Chao Cai , Jianping Wang , Aifei Wang , Youjia Xu , Yanwen Fang , Min Wei , Dachuan Yin , Xinle Luo , Ming Gong , Hao Zhang , Peng Shang","doi":"10.1016/j.jot.2024.10.012","DOIUrl":"10.1016/j.jot.2024.10.012","url":null,"abstract":"<div><h3>Objective</h3><div>Clinical studies, epidemiological investigations and animal experiments have demonstrated that iron overload lead to bone loss, especially postmenopausal osteoporosis. As a physiotherapy tool, electromagnetic fields already used in clinical treatment of osteoporosis and participates in bone remodeling by affecting the iron metabolism of organisms. As an electromagnetic field with constant magnetic flux density and direction, the mechanism of static magnetic field (SMF) regulating iron metabolism remains unclear. Therefore, the aim of this study was to investigate the effects of moderate static magnetic field (MMF) on iron metabolism and bone metabolism in postmenopausal osteoporosis and <em>HAMP</em>-deficient mouse models, and to elucidate the underlying mechanisms.</div></div><div><h3>Methods</h3><div>Firstly, the effects of MMF on bone metabolism and iron metabolism in 22 postmenopausal osteoporosis participants were evaluated by comparing the changes of bone mineral density (BMD) and serum ferritin before and after treatment. Secondly, 10-week-old male C57BL/6 <em>HAMP</em><sup>+/+</sup> and <em>HAMP</em><sup>−/−</sup> mice were randomly divided into four groups, namely GMF-<em>HAMP</em><sup>+/+</sup> group and MMF-<em>HAMP</em><sup>+/+</sup> group, GMF-<em>HAMP</em><sup>−/−</sup> group and MMF-<em>HAMP</em><sup>−/−</sup> group (n = 8/group). The MMF-treated mice were exposed daily to MMF, while the remaining group was exposed to geomagnetic field (GMF) for 8 weeks. BMD was scanned and bone tissues were collected for mechanical, structural and histological analysis. In addition, analysis of serum and tissue iron content evaluated the regulation of systemic iron metabolism by MMF. Finally, the effects of MMF on the differentiation of primary macrophages and primary osteoblasts were evaluated <em>in vitro</em>.</div></div><div><h3>Results</h3><div>In clinical trial, MMF decreased serum ferritin levels in postmenopausal osteoporosis patients, which was negatively correlated with changes in lumbar BMD. <em>In vivo</em>, the results showed that <em>HAMP</em>-deficient mice were accompanied by iron overload, along with reduced lumbar vertebra bone mass and bone quality. MMF improved the bone mass, microstructure and biomechanical properties of lumbar vertebrae in <em>HAMP</em><sup>−/−</sup> mice. <em>In vitro</em>, MMF reduced the number and differentiation of osteoclasts in <em>HAMP</em><sup>−/−</sup> mice, and promoted primary osteoblast differentiation by activating Wnt/β-catenin signaling pathway. Further, MMF also reduced the iron ion conversion and enhanced the antioxidant system of <em>HAMP</em><sup>−/−</sup> mice. These data suggested that MMF could regulate iron metabolism and salvage bone loss caused by iron accumulation.</div></div><div><h3>Conclusions</h3><div>The clinical trial and laboratory results suggested that MMF intervention has a protective effect on bone loss caused by iron metabolism disorders.</di","PeriodicalId":16636,"journal":{"name":"Journal of Orthopaedic Translation","volume":"50 ","pages":"Pages 144-157"},"PeriodicalIF":5.9,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143179168","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"OGT mediated HDAC5 O-GlcNAcylation promotes osteogenesis by regulating the homeostasis of epigenetic modifications and proteolysis","authors":"Yu Du ,&nbsp;Xiang Gao ,&nbsp;Jianqiang Chen ,&nbsp;Xinxin Chen ,&nbsp;Hang Liu ,&nbsp;Wenge He ,&nbsp;Lu Liu ,&nbsp;Yue Jiang ,&nbsp;Baicheng He ,&nbsp;Zhongliang Deng ,&nbsp;Chao Liang ,&nbsp;Fengjin Guo","doi":"10.1016/j.jot.2024.10.004","DOIUrl":"10.1016/j.jot.2024.10.004","url":null,"abstract":"<div><h3>Background</h3><div>O-GlcNAc transferase (OGT) is responsible for attaching O-linked N-acetylglucosamine (O-GlcNAc) to proteins, regulating diverse cellular processes ranging from transcription and translation to signaling and metabolism. This study focuses on the role and mechanisms of OGT in osteogenesis.</div></div><div><h3>Materials and methods</h3><div>We found that OGT is downregulated in osteoporosis by bioinformatics analysis, determined its role in osteogenic differentiation by using OGT inhibitors (or OGA inhibitors) as well as conditional knockout OGT mice in <em>vitro</em> and in <em>vivo</em>, and explored and specific mechanisms by quantitative proteomic analysis and RNA-seq, qRT-PCR, western blotting, immunofluorescence, H&amp;E, ALP, ARS, Masson staining, IHC, micro CT, etc.</div></div><div><h3>Results</h3><div>we revealed that OGT positively influenced osteogenesis and osteoblast differentiation in <em>vitro</em> as well as ovariectomy (OVX) mice in <em>vivo</em>. Consistently, mice with conditionally depleted OGT exhibited a reduction in bone mass, while O-GlcNAcylation enhancer could partially recover bone mass in ovariectomy (OVX) mice. Mechanistically, quantitative proteomic analysis and high-throughput RNAseq further reveals that HDAC5 is one of the endogenous O-GlcNAcylation substrates, and O-GlcNAcylation of HDAC5 on Thr934 promotes its translocation to lysosomes and subsequent degradation, thus, elevating the O-GlcNAcylation level of HDAC5 leads to its cytoplasmic cleavage, consequently diminished its nuclear entry and enhanced DNA transcription. The OGT-mediated O-GlcNAcylation of HDAC5 modulates the balance between its cytoplasmic proteolysis and nuclear entry, thereby impacting the Notch signaling pathway and DNA epigenetic modifications then playing a role in osteogenesis.</div></div><div><h3>Conclusion</h3><div>OGT is a regulator that promotes osteoblast differentiation and bone regeneration. Additionally, it highlights the critical function of HDAC5 O-GlcNAcylation in controlling epigenetics. This study offers fresh perspectives on osteogenesis and O-GlcNAcylation, proposing that the OGT-mediated O-GlcNAcylation of HDAC5 could be a promising target for osteoporosis treatment.</div></div><div><h3>The translational potential of this article</h3><div>On one side, OGT might potentially be used as a new biomarker for clinical diagnosis of osteoporosis (OP) in the future. On the other side, small molecule inhibitors of HDAC5, a glycosylation substrate of OGT, or OGT agonists such as silymarin, could all potentially serve as therapeutic targets for the prevention or treatment of OP in the future.</div></div>","PeriodicalId":16636,"journal":{"name":"Journal of Orthopaedic Translation","volume":"50 ","pages":"Pages 14-29"},"PeriodicalIF":5.9,"publicationDate":"2024-11-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142703343","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Paeonol inhibits ACSL4 to protect chondrocytes from ferroptosis and ameliorates osteoarthritis progression","authors":"Siyang Cao ,&nbsp;Yihao Wei ,&nbsp;Ao Xiong ,&nbsp;Yaohang Yue ,&nbsp;Jun Yang ,&nbsp;Deli Wang ,&nbsp;Xiyu Liu ,&nbsp;Hui Zeng ,&nbsp;Dongquan Shi ,&nbsp;Ye Li","doi":"10.1016/j.jot.2024.10.005","DOIUrl":"10.1016/j.jot.2024.10.005","url":null,"abstract":"<div><h3>Background</h3><div>Discovering an inhibitor for acyl-CoA synthetase long-chain family member 4 (ACSL4), a protein that triggers cell injury via ferroptosis, presents potential to minimize cellular damage. This study investigates paeonol (PAE), a traditional Chinese herbal medicine, as an ACSL4 inhibitor to prevent chondrocyte ferroptosis and protect against osteoarthritis (OA).</div></div><div><h3>Methods</h3><div>We conducted <em>in vitro</em> experiments using mouse chondrocytes treated with PAE to mitigate ferroptosis induced by Interleukin-1 Beta (IL-1β) or ferric ammonium citrate (FAC), examining intracellular ferroptotic indicators, cartilage catabolic markers, and ferroptosis regulatory proteins. A mouse OA model was created via destabilized medial meniscus (DMM), followed by intra-articular PAE injections. After 8 weeks, micro-computed tomography and histological assessments evaluated PAE's protective and anti-ferroptotic effects in the OA model.</div></div><div><h3>Results</h3><div><em>In vitro</em> results showed PAE significantly reduced IL-1β/FAC-induced damage by targeting ACSL4, including cell apoptosis, inflammatory responses, extracellular matrix degradation, and ferroptotic markers (oxidative stress, lipid peroxidation, and iron buildup). It also restored the expression of ferroptotic suppressors and mitigated mitochondrial damage. Additionally, PAE increased cartilage anabolic marker expression while reducing cartilage catabolic marker expression. Molecular docking, cellular thermal shift assay, and drug affinity responsive target stability analysis verified the binding interaction between PAE and ACSL4. Furthermore, the role of PAE in chondrocytes was further verified through ACSL4 knockdown and overexpression. <em>In vivo</em>, mice with OA showed increased cartilage degradation and ferroptosis, while intra-articular PAE injection alleviated these pathological changes.</div></div><div><h3>Conclusion</h3><div>PAE significantly protects chondrocytes from ferroptosis induced by IL-1β/FAC in primary mouse chondrocytes and DMM surgery-induced OA mice through ACSL4 inhibition.</div></div><div><h3>The translational potential of this article</h3><div>These findings highlight the potential of targeting ACSL4 in chondrocytes as a treatment strategy for OA, positioning PAE as a promising drug candidate.</div></div>","PeriodicalId":16636,"journal":{"name":"Journal of Orthopaedic Translation","volume":"50 ","pages":"Pages 1-13"},"PeriodicalIF":5.9,"publicationDate":"2024-11-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142703790","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Zhuangyao Jianshen Wan ameliorates senile osteoporosis in SAMP6 mice through Modulation of the GCN5L1-mediated PI3K/Akt/wnt signaling pathway","authors":"Shaoyong Ma ,&nbsp;Jian Lin ,&nbsp;Meng Yang ,&nbsp;JiaJia Wang ,&nbsp;Lujiao Lu ,&nbsp;Ying Liang ,&nbsp;Yan Yang ,&nbsp;Yanzhi Liu ,&nbsp;Dongtao Wang ,&nbsp;Yajun Yang","doi":"10.1016/j.jot.2024.08.009","DOIUrl":"10.1016/j.jot.2024.08.009","url":null,"abstract":"&lt;div&gt;&lt;h3&gt;Background&lt;/h3&gt;&lt;div&gt;Senile osteoporosis (SOP) is a systemic bone disease characterized by increased susceptibility to fractures. However, there is currently no effective treatment for SOP. The Zhuangyao Jianshen Wan (ZYJSW) pill is traditionally believed to possess kidney-nourishing and bone-strengthening effects, demonstrating efficacy in treating fractures. Despite this, its effectiveness and mechanism in SOP remain unclear. This study aims to investigate the therapeutic potential of ZYJSW in treating SOP in senescence accelerated mouse prone 6 (SAMP6, P6) mice, and elucidate the underlying mechanisms.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Methods&lt;/h3&gt;&lt;div&gt;Four-month-old SAMP6 mice were categorized into six groups: the model group (SAMP6), low, medium, and high-dose ZYJSW treatment groups, calcitriol treatment (positive control 1) group, and metformin treatment (positive control 2) group. Gastric administration was carried out for 15 weeks, and a normal control group comprising four-month-old Senescence-Accelerated Mouse Resistant 1 (SAMR1) mice. Changes in body weight, liver and kidney function, bone protective effects, and muscle quality were evaluated using various assays, including H&amp;E staining, Goldner staining, bone tissue morphology analysis, Micro-CT imaging, and biomechanical testing. Qualitative analysis and quality control of ZYJSW were performed via LC-MS/MS analysis. To explore mechanisms, network pharmacology and proteomics were employed, and the identified proteins were validated by Western blotting.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Results&lt;/h3&gt;&lt;div&gt;Oral administration of ZYJSW to P6 mice exerted preventive efficacy against osteopenia, impaired bone microstructure, and poor bone and muscle quality. ZYJSW attenuated the imbalance in bone metabolism by promoting bone formation, as evidenced by the upregulation of key factors such as Runt-related transcription factor 2 (RUNX2), Bone Morphogenetic Protein (BMP2), Osteoprotegerin (OPG) and Osteocalcin (OCN), while simultaneously inhibiting bone resorption through the downregulation of TNF receptor associated factor 6 (TRAF6), Tartrate resistant acid phosphatase (TRAP), Receptor activator for nuclear factor-κB ligand (RANKL) and Cathepsin K (CTSK). Additionally, ZYJSW enhanced muscle structure and function by counteracting the elevation of Ubiquitin (Ub), Muscle RING-finger protein-1 (Murf-1), F-Box Protein 32 (FBOX32), and Myogenin (Myog). Network pharmacology predictions, proteomics analysis corroborated by published literature demonstrated the role of ZYJSW involving in safeguarding mitochondrial biogenesis. This was achieved by suppressing GCN5L1 expression, contributing to the heightened expression of TFAM, PGC-1α, and nuclear respiratory factor-1 (NRF-1) proteins. ZYJSW also positively modulated Wnt signaling pathways responsible for bone formation, due to regulating expressions of key components like β-catenin, GSK-3β, and LRP5. In addition, ZYJSW causes the downregulation of the PI3K/Akt pathway","PeriodicalId":16636,"journal":{"name":"Journal of Orthopaedic Translation","volume":"49 ","pages":"Pages 308-324"},"PeriodicalIF":5.9,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142587281","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"New developments in osteoporosis, osteoarthritis and soft tissue repair","authors":"Gang Li (Prof)","doi":"10.1016/j.jot.2024.11.002","DOIUrl":"10.1016/j.jot.2024.11.002","url":null,"abstract":"","PeriodicalId":16636,"journal":{"name":"Journal of Orthopaedic Translation","volume":"49 ","pages":"Pages A1-A2"},"PeriodicalIF":5.9,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11681327/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142903094","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum to ‘Osteostaticytes: A novel osteoclast subset couples bone resorption and bone formation’[Journal of Orthopaedic Translation 47 (2024) 144–160]","authors":"Zhiyuan Wei ,&nbsp;Jian Zhou ,&nbsp;Jie Shen ,&nbsp;Dong Sun ,&nbsp;Tianbao Gao ,&nbsp;Qin Liu ,&nbsp;Hongri Wu ,&nbsp;Xiaohua Wang ,&nbsp;Shulin Wang ,&nbsp;Shiyu Xiao ,&nbsp;Chao Han ,&nbsp;Di Yang ,&nbsp;Hui Dong ,&nbsp;Yuzhang Wu ,&nbsp;Yi Zhang ,&nbsp;Shuai Xu ,&nbsp;Xian Wang ,&nbsp;Jie Luo ,&nbsp;Qijie Dai ,&nbsp;Jun Zhu ,&nbsp;Zhao Xie","doi":"10.1016/j.jot.2024.08.018","DOIUrl":"10.1016/j.jot.2024.08.018","url":null,"abstract":"","PeriodicalId":16636,"journal":{"name":"Journal of Orthopaedic Translation","volume":"49 ","pages":"Pages 339-340"},"PeriodicalIF":5.9,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11681331/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142903086","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Recent developments in Achilles tendon risk-analyzing rupture factors for enhanced injury prevention and clinical guidance: Current implications of regenerative medicine","authors":"Maria V. Sankova ,&nbsp;Narasimha M. Beeraka ,&nbsp;Marine V. Oganesyan ,&nbsp;Negoriya A. Rizaeva ,&nbsp;Aleksey V. Sankov ,&nbsp;Olga S. Shelestova ,&nbsp;Kirill V. Bulygin ,&nbsp;Hemanth Vikram PR ,&nbsp;A.N. Barinov ,&nbsp;A.K. Khalimova ,&nbsp;Y. Padmanabha Reddy ,&nbsp;Basappa Basappa ,&nbsp;Vladimir N. Nikolenko","doi":"10.1016/j.jot.2024.08.024","DOIUrl":"10.1016/j.jot.2024.08.024","url":null,"abstract":"&lt;div&gt;&lt;h3&gt;Background&lt;/h3&gt;&lt;div&gt;In recent years, many countries have actively implemented programs and strategies to promote physical education and sports. Despite these efforts, the increase in physical activity has been accompanied by a significant rise in muscle and tendon-ligament injuries, with Achilles tendon rupture being the most prevalent, accounting for 47 % of such injuries. This review aims to summarize all significant factors determining the predisposition of the Achilles tendon to rupture, to develop effective personalized prevention measures.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Objective&lt;/h3&gt;&lt;div&gt;To identify and evaluate the risk factors contributing to Achilles tendon rupture and to develop strategies for personalized prevention.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Methods&lt;/h3&gt;&lt;div&gt;This review utilized data from several databases, including Elsevier, Global Health, PubMed-NCBI, Embase, Medline, Scopus, ResearchGate, RSCI, Cochrane Library, Google Scholar, eLibrary.ru, and CyberLeninka. Both non-modifiable and modifiable risk factors for Achilles tendon injuries and ruptures were analyzed.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Results&lt;/h3&gt;&lt;div&gt;The analysis identified several non-modifiable risk factors, such as genetic predisposition, anatomical and functional features of the Achilles tendon, sex, and age. These factors should be considered when selecting sports activities and designing training programs. Modifiable risk factors included imbalanced nutrition, improper exercise regimens, and inadequate monitoring of Achilles tendon conditions in athletes. Early treatment of musculoskeletal injuries, Achilles tendon diseases, foot deformities, and metabolic disorders is crucial. Long-term drug use and its risk assessment were also highlighted as important considerations. Furthermore, recent clinical advancements in both conventional and surgical methods to treat Achilles tendon injuries were described. The efficacy of these therapies in enhancing functional outcomes in individuals with Achilles injuries was compared. Advancements in cell-based and scaffold-based therapies aimed at enhancing cell regeneration and repairing Achilles injuries were also discussed.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Discussion&lt;/h3&gt;&lt;div&gt;The combination of several established factors significantly increases the risk of Achilles tendon rupture. Addressing these factors through personalized prevention strategies can effectively reduce the incidence of these injuries. Proper nutrition, regular monitoring, timely treatment, and the correction of metabolic disorders are essential components of a comprehensive prevention plan.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Conclusion&lt;/h3&gt;&lt;div&gt;Early identification of Achilles tendon risk factors allows for the timely development of effective personalized prevention strategies. These measures can contribute significantly to public health preservation by reducing the incidence of Achilles tendon ruptures associated with physical activity and sports. Continued research and clinical advancements in treatment me","PeriodicalId":16636,"journal":{"name":"Journal of Orthopaedic Translation","volume":"49 ","pages":"Pages 289-307"},"PeriodicalIF":5.9,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142578322","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Innovative development of robot reduction system in geriatric pelvic fractures: A single-center case series in Beijing, China","authors":"Chunpeng Zhao ,&nbsp;Honghu Xiao ,&nbsp;Qiyong Cao ,&nbsp;Yufeng Ge ,&nbsp;Yuneng Li ,&nbsp;Yu Wang ,&nbsp;Gang Zhu ,&nbsp;Xinbao Wu","doi":"10.1016/j.jot.2024.08.023","DOIUrl":"10.1016/j.jot.2024.08.023","url":null,"abstract":"<div><div>Displaced fragility fractures of the pelvis (FFP) pose significant challenges in orthopaedic trauma, owing to patient comorbidities, deteriorating bone quality, and surgical complexities. Despite technological advancements, no robotic methods have been documented for displaced FFP management. To address this, we introduced an advanced robot-assisted fracture reduction system, comprising a tracking device, path planning software, and robotic arms. This study evaluated fifteen consecutive patients with displaced FFP (average age 80.4 ± 9.1 years), who underwent robot-assisted reduction and internal fixation (RARIF) between January 2022 and May 2023. All were categorized as Rommens FFP type III, with a median time of 6 days (range 4–11) from injury to surgery. Operative times averaged 165 ± 44 min, with median blood loss of 50 mL. Postoperative radiographs showed all patients achieved excellent or good reductions as per Matta criteria, marking a 100 % success rate. A 6-month follow-up revealed an average modified Majeed score of 81.4, with 85.7 % of patients rated excellent or good. All fractures healed without complications. Leveraging our intelligent system, RARIF proves to be a safe and effective approach for displaced FFP, facilitating postoperative pain alleviation and early mobilization despite compromised health and bone conditions. This approach may revolutionize the management of FFP in an increasingly aging population, signaling a significant shift in therapeutic strategies.</div><div>Translational Potential of this Article: Elderly patients with displaced FFP often present complex surgical challenges due to comorbidities and poor bone quality, complicating reduction procedures and often leading to ineffective fixation. Addressing these challenges, we have developed an innovative robot-assisted fracture reduction system, offering a practical alternative to conventional methods. This system optimizes the applied force and direction during the reduction process, thereby reducing the needs for manual and repetitive attempts. Our report, detailing the successful implementation of this technique in 15 FFP cases, signifies a considerable leap forward in the field of orthopaedic surgery. This technique notably benefits the elderly population, a group traditionally marginalized in receiving care for complex orthopedic conditions.</div></div>","PeriodicalId":16636,"journal":{"name":"Journal of Orthopaedic Translation","volume":"49 ","pages":"Pages 283-288"},"PeriodicalIF":5.9,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142554142","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sensory nerve EP4 facilitates heterotopic ossification by regulating angiogenesis-coupled bone formation","authors":"Rongmin Lin ,&nbsp;Hancheng Lin ,&nbsp;Chencheng Zhu ,&nbsp;Jieming Zeng ,&nbsp;Jiahui Hou ,&nbsp;Ting Xu ,&nbsp;Yihui Tan ,&nbsp;Xuyou Zhou ,&nbsp;Yuan Ma ,&nbsp;Mankai Yang ,&nbsp;Kuanhai Wei ,&nbsp;Bin Yu ,&nbsp;Hangtian Wu ,&nbsp;Zhuang Cui","doi":"10.1016/j.jot.2024.09.005","DOIUrl":"10.1016/j.jot.2024.09.005","url":null,"abstract":"<div><h3>Objective</h3><div>Heterotopic ossification (HO) refers to the abnormal development of bone in soft tissue rather than within bone itself. Previous research has shown that sensory nerve prostaglandin E2 receptor 4 (EP4) signaling not only governs pain perception but also influences bone formation. However, the relationship between sensory nerve EP4 and the pathogenesis of HO in the Achilles tendon remains unclear. This study aims to investigate this relationship and the underlying mechanisms.</div></div><div><h3>Methods</h3><div>We generated sensory nerve EP4-specific knockout mice, with the genotype of Avil-CreEP4^fl/fl, was propagated. Transcriptome sequencing and bioinformatics analysis techniques were used to identify the potential molecular pathways involving with sensory nerve EP4. Additionally, a neurectomy mouse model was created by transecting the sciatic nerve transection, to examine the effects and mechanisms of peripheral innervation on HO in vivo. Micro-CT, immunofluorescence (IF), Hematoxylin and Eosin (H&amp;E) Staining, Safranin O-Fast Green staining and western blotting were used to analyze changes in cellular and tissue components.</div></div><div><h3>Results</h3><div>We here observed an increase in sensory nerve EP4 and H-type vessels during the pathogenesis of HO in both human subjects and mice. Proximal neurectomy through sciatic nerve transection or the targeted knockout of EP4 in sensory nerves hindered angiogenesis-dependent bone formation and the development of HO at the traumatic site of the Achilles tendon. Furthermore, we identified the Efnb2 (Ephrin-B2)/Dll4 (Delta-like ligand 4) axis as a potential downstream element influenced by sensory nerve EP4 in the regulation of HO. Notably, administration of an EP4 inhibitor demonstrated the ability to alleviate HO. Based on these findings, sensory nerve EP4 emerges as an innovative and promising approach for managing HO.</div></div><div><h3>Conclusion</h3><div>Our findings demonstrate that the sensory nerve EP4 promotes ectopic bone formation by modulating angiogenesis-associated osteogenesis during HO.</div></div><div><h3>The translational potential of this article</h3><div>Our results provide a mechanistic rationale for targeting sensory nerve EP4 as a promising candidate for HO therapy.</div></div>","PeriodicalId":16636,"journal":{"name":"Journal of Orthopaedic Translation","volume":"49 ","pages":"Pages 325-338"},"PeriodicalIF":5.9,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142587282","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}