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Ubiquitin-specific protease 26 facilitates endochondral ossification by driving chondrocyte hypertrophy and mineralization 认领 引用
1
作者 Changwei Li Yiming Xu +6 位作者 Li Zhou Leilei Chang Zhou Dan Yunhe Jiang Chao Wang Lianfu Deng Guoqing Tang 《Bone Research》 SCIE CAS CSCD 2026年第3期963-980,共18页
Chondrocyte hypertrophy and mineralization are essential for endochondral ossification;however,the mechanisms underlying these processes remain incompletely understood.In this study,we have identified the facilitated ... Chondrocyte hypertrophy and mineralization are essential for endochondral ossification;however,the mechanisms underlying these processes remain incompletely understood.In this study,we have identified the facilitated role of ubiquitin-specific protease 26(USP26)in endochondral ossification by stimulating chondrocyte hypertrophy and mineralization.Ultimately,this promotes skeletal development,bone fracture healing,and the occurrence of osteoarthritis.Mechanistically,USP26 decreases FBP2 undergoing K63-linked ubiquitination,leading to a reduction in the protein level of FBP2.This reduction promotes mitochondrial biogenesis and oxidative phosphorylation,thus facilitating chondrocyte hypertrophy and mineralization and aiding in the process of endochondral ossification.Furthermore,our study found that compression loading induces USP26 to initiate chondrocyte hypertrophy and mineralization through the phosphorylation of estrogen receptor-αat serine 118.These findings suggest that USP26,acting as a mechanosensor,facilitates chondrocyte hypertrophy and mineralization by maintaining mitochondrial biogenesis through the reduction of FBP2.Identifying USP26 as a potential therapeutic target for physiological skeletal growth,bone fracture healing,and osteoarthritis. 展开更多
关键词 endochondral ossificationhoweverthe mitochondrial biogenesis chondrocyte hypertrophy ubiquitin specific protease endochondral ossification skeletal developmentbone mineralization
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M1 macrophage-derived CXCL12 drives neurogenic heterotopic ossification following spinal cord injury 认领 引用
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作者 Yulei Xie Yaomin Luo +3 位作者 Xin Chen Yinxu Wang Wei Song Hua Ling 《Neural Regeneration Research》 SCIE CAS CSCD 2026年第10期4965-4977,共13页
Patients with spinal cord injury frequently develop neurogenic heterotopic ossification,whose pathogenesis remains incompletely understood.Existing research models struggle to accurately simulate the complex pathologi... Patients with spinal cord injury frequently develop neurogenic heterotopic ossification,whose pathogenesis remains incompletely understood.Existing research models struggle to accurately simulate the complex pathological process.To establish a reliable neurogenic heterotopic ossification research model,elucidate its pathogenesis,and explore early intervention strategies,this study successfully developed a spinal cord injury-induced neurogenic heterotopic ossification mouse model.Significant ectopic bone formation,restricted hip and knee joint mobility,and motor dysfunction were observed,accompanied by elevated expression of the osteogenic markers alkaline phosphatase,runt-related transcription factor 2,sex-determining region Y-box 9,and osteocalcin.Proteomics and quantitative polymerase chain reaction analysis revealed upregulation of chemokine(C-X-C motif)ligand(CXCL)12,C-X-C chemokine receptor type 4(CXCR4),and LYN proto-oncogene,whereas CXCL1 was downregulated in the neurogenic heterotopic ossification group.In vivo experiments confirmed abnormal accumulation of M1 macrophages in muscles surrounding early ectopic bone tissue,with markedly elevated CXCL12 expression.In vitro studies further revealed that M1 macrophages are the primary source of CXCL12 secretion,and their cell culture supernatants promote the proliferation,migration,and osteoblastic differentiation potential of bone marrow mesenchymal stem cells.Mechanistically,CXCL12 activates the phosphatidylinositol 3-kinase/protein kinase B pathway by binding to the CXCR4 receptor,thereby driving the osteogenic differentiation of bone marrow mesenchymal stem cells.These findings indicate a causal relationship between the pathological process of neurogenic heterotopic ossification following spinal cord injury and the activation of the CXCL12-CXCR4-phosphatidylinositol 3-kinase-protein kinase B signaling axis,which modulates bone marrow mesenchymal stem cell function through M1 macrophage polarization.This study reveals a key mechanism driving the osteogenic differentiation of bone marrow mesenchymal stem cells,providing new directions for early warning and targeted treatment of neurogenic heterotopic ossification following spinal cord injury. 展开更多
关键词 CXCL12 CXCR4 heterotopic ossification macrophage migration mineralization osteogenic PI3K/AKT proliferation spinal cord injury
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APEX1,a transcriptional hub for endochondral ossification and fracture repair 认领 引用
3
作者 José Valdés-Fernández Miguel Echanove-González de Anleo +10 位作者 Juan Antonio Romero-Torrecilla Tania López-Martínez Purificación Ripalda-Cemboráin María Erendira Calleja-Cervantes Asier Ullate-Agote Elena Iglesias Belén Prados-Pinto JoséLuis de la Pompa Felipe Prósper Emma Muiños-López Froilán Granero-Moltó 《Bone Research》 SCIE CAS CSCD 2026年第1期179-194,共16页
After injury,bone tissue initiates a reparative response to restore its structure and function.The failure to initiate or delay this response could result in fracture nonunion.The molecular mechanisms underlying the o... After injury,bone tissue initiates a reparative response to restore its structure and function.The failure to initiate or delay this response could result in fracture nonunion.The molecular mechanisms underlying the occurrence of fracture nonunion are not yet established.We propose that hypoxia-triggered signaling pathways,mediated by reactive oxygen species(ROS)homeostasis,control Bmp2 expression and fracture healing initiation.The excessive ROS leads to oxidative stress and,ultimately,fracture nonunion.In this study,we silenced Apex1,the final ROS signaling transducer that mediates the activation of key transcription factors by their cysteines oxidoreduction,evaluating its role during endochondral ossification and fracture repair.Silencing Apex1 in limb bud mesenchyme results in transient metaphyseal dysplasia derived from impaired chondrocyte differentiation.During bone regeneration,Apex1 silencing induces a fracture nonunion phenotype,characterized by delayed fracture repair initiation,impaired periosteal response,and reduced chondrocyte and osteoblast differentiation.This compromised chondrocyte differentiation hampers callus vascularization and healing progression.Our findings highlight a critical mechanism where hypoxia-driven ROS signaling in mesenchymal progenitors through APEX1 is essential for fracture healing initiation. 展开更多
关键词 reactive oxygen species ros homeostasiscontrol endochondral ossification molecular mechanisms fracture repair apex reactive oxygen species hypoxia reparative response
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Machine learning identifies complement factor I as a shared mediator of periodontitis and ossification of posterior longitudinal ligament 认领 引用
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作者 Yu-Nan Man Lu-Yang Zhong +1 位作者 Yue-Liang Wen Mao-Lin He 《World Journal of Orthopedics》 2026年第3期133-151,共19页
BACKGROUND The clinical co-occurrence of periodontitis and ossification of the posterior longitudinal ligament(OPLL)suggests shared pathophysiological mechanisms,which remain poorly understood.AIM To elucidate the key... BACKGROUND The clinical co-occurrence of periodontitis and ossification of the posterior longitudinal ligament(OPLL)suggests shared pathophysiological mechanisms,which remain poorly understood.AIM To elucidate the key molecular and cellular mechanisms between periodontitis and OPLL.METHODS Transcriptomic datasets for human periodontitis and OPLL were integrated.We performed differential gene expression analysis,weighted gene co-expression network analysis,and cross-dataset meta-analysis.A comprehensive machine learning framework incorporating 10 algorithms was applied to identify core genes,with model interpretability assessed via SHapley Additive exPlanations.Single-cell RNA sequencing data from periodontitis tissues were used to validate cell-type-specific expression,and functional enrichment analyses were conducted to elucidate relevant pathways.RESULTS Multi-step analysis identified complement factor I(CFI)as a principal contributor to both conditions.CFI expression was consistently upregulated and demonstrated strong discriminatory capacity for periodontitis.At single-cell resolution,endothelial cells within the periodontitis microenvironment were observed to express CFI.Functional enrichment analysis indicated that CFI-positive cells were involved in pathways related to cell adhesion(focal adhesion,adherens junctions),inflammatory signaling(PI3K-Akt pathway),and bacterial infection responses.CONCLUSION CFI was identified as a pivotal node connecting periodontitis and OPLL,revealing novel mechanisms and suggesting its potential as a biomarker and therapeutic target. 展开更多
关键词 Ossification of the posterior longitudinal ligament Periodontitis Complement factor I Discriminatory biomarker Machine learning Transcriptome Single-cell RNA sequencing
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PRMT6 is required for initiating and amplifying macrophage-induced inflammation in heterotopic ossification by increasing CCL2 expression 认领 引用
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作者 Wenxiang Chu Weilin Peng +8 位作者 Zhengqiang Wu Yu Xiong Zhongya Gao Yang Li Bangke Zhang Liang Wang Haibin Wang Chaofeng Han Xuhua Lu 《Bone Research》 SCIE CAS CSCD 2026年第2期625-639,共15页
Heterotopic ossification(HO)is a debilitating disorder marked by ectopic bone formation in soft tissues,frequently triggered by inflammation after trauma.While macrophage-driven inflammation plays a critical role in H... Heterotopic ossification(HO)is a debilitating disorder marked by ectopic bone formation in soft tissues,frequently triggered by inflammation after trauma.While macrophage-driven inflammation plays a critical role in HO pathogenesis,the molecular mechanisms governing its initiation,amplification and resolution remain elusive.Using a trauma/burn injury(TBI)-induced mouse model of HO,we identified rapid and sustained macrophage accumulation at the injury site during the early inflammatory phase,and macrophage depletion markedly suppressed HO formation.Transcriptomic profiling identified a pronounced upregulation of protein arginine methyltransferase 6(PRMT6)in macrophages following injury.Genetic deletion or macrophage-targeted knockdown of Prmt6 reduced macrophage accumulation and significantly attenuated HO,without impairing tendon repair.Consistently,pharmacological inhibition of PRMT6 suppressed HO only when administered during the early inflammatory phase,indicating a restricted therapeutic window.Mechanistically,PRMT6 amplified macrophage chemotactic signaling by transcriptionally and epigenetically upregulating CCL2.Genetic disruption of macrophage-derived CCL2 phenocopied Prmt6 deficiency,whereas CCL2 supplementation rescued macrophage recruitment and partially restored HO in Prmt6-deficient mice.At the molecular level,PRMT6 formed a coactivation complex with NF-κB and catalyzed H3R17 asymmetric dimethylation at the Ccl2 promoter,thereby promoting sustained chemokine expression.Collectively,our findings identify PRMT6 as a central epigenetic amplifier of macrophage-driven inflammation that links early injury responses to ectopic bone formation.Targeting PRMT6 during the early inflammatory phase represents a promising strategy to prevent HO while preserving physiological tissue repair. 展开更多
关键词 heterotopic ossification ho soft tissuesfrequently molecular mechanisms macrophage inflammation ectopic bone formation prmt ccl
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Polycystin-1 regulates tendon-derived mesenchymal stem cells fate and matrix organization in heterotopic ossification 认领 引用 被引量：3
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作者 Yi Li Xu Mei Huang +8 位作者 Yang Zhang Xin Ying Su Min Huang Nan Yu Zou Yu Rui Jiao Yu Chen Sun Ling Liu Yong Hua Lei Chang Jun Li 《Bone Research》 SCIE CAS CSCD 2025年第1期183-196,共14页
Mechanical stress modulates bone formation and organization of the extracellular matrix(ECM),the interaction of which affects heterotopic ossification(HO).However,the mechanically sensitive cell populations in HO and ... Mechanical stress modulates bone formation and organization of the extracellular matrix(ECM),the interaction of which affects heterotopic ossification(HO).However,the mechanically sensitive cell populations in HO and the underlying mechanism remain elusive.Here,we show that the mechanical protein Polysyctin-1(PC1,Pkd1)regulates CTSK lineage tendon-derived mesenchymal stem cell(TDMSC)fate and ECM organization,thus affecting HO progression.First,we revealed that CTSK lineage TDMSCs are the major source of osteoblasts and fibroblasts in HO and are responsive to mechanical cues via single-cell RNA sequencing analysis and experiments with a lineage tracing mouse model.Moreover,we showed that PC1 mediates the mechanosignal transduction of CTSK lineage TDMSCs to regulate osteogenic and fibrogenic differentiation and alters the ECM architecture by facilitating TAZ nuclear translocation.Conditional gene depletion of Pkd1 or Taz in CTSK lineage cells and pharmaceutical intervention in the PC1-TAZ axis disrupt osteogenesis,fibrogenesis and ECM organization,and consequently attenuate HO progression.These findings suggest that mechanically sensitive CTSK-lineage TDMSCs contribute to heterotopic ossification through PC1-TAZ signaling axis mediated cell fate determination and ECM organization. 展开更多
关键词 ossification heterotopic tendon
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SMN deficiency inhibits endochondral ossification via promoting TRAF6-induced ubiquitination degradation of YBX1 in spinal muscular atrophy 认领 引用
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作者 Zijie Zhou Xinbin Fan +6 位作者 Taiyang Xiang Yinxuan Suo Xiaoyan Shi Yaoyao Li Yimin Hua Lei Sheng Xiaozhong Zhou 《Bone Research》 SCIE CAS CSCD 2025年第6期1552-1568,共17页
Survival of motor neuron(SMN)protein encoded by SMN1 gene,is the essential and ubiquitously expressed protein in all tissues.Prior studies demonstrated that SMN deficiency impaired bone development,but the underlying ... Survival of motor neuron(SMN)protein encoded by SMN1 gene,is the essential and ubiquitously expressed protein in all tissues.Prior studies demonstrated that SMN deficiency impaired bone development,but the underlying mechanism of abnormal endochondral ossification remains obscure.Here,we showed SMN is involved in hypertrophic chondrocytes differentiation through regulating RNA splicing and protein degradation via analyzing single cell RNA-sequencing data of hypertrophic chondrocytes.Of note,SMN loss induced dwarfism and delayed endochondral ossification in Smn1 depletion-severe spinal muscular atrophy(SMA)mouse model and Smn1 chondrocyte conditional knockdown mouse.Histological analysis revealed that SMN deficiency expanded the zone of hypertrophic chondrocytes in the growth plates,but delayed turnover from hypertrophic to ossification zone.Widespread changes in endochondral ossification related gene expression and alternative splicing profiles were identified via RNA sequencing of growth plate cartilages from SMA mice on postnatal day 4.Importantly,Mass spectrometry-based proteomics analysis elucidated Y-box-binding protein 1(YBX1)as a vital SMN-binding factor,was decreased in SMA mice.YBX1 knockdown reproduced the aberrant gene expression and splicing changes observed in SMA growth plate cartilages.Comparing the binding proteins of SMN and YBX1 revealed TNF receptor-associated factor 6(TRAF6),which promoted ubiquitination degradation of YBX1.By conditionally deleting Smn1 in chondrocytes of WT mice and overexpressing Smn1 in chondrocytes of SMA mice,we proved that SMN expression in chondrocytes is critical for hypertrophic chondrocyte-mediated endochondral ossification.Collectively,these results demonstrate that SMN deficiency contributes to rapid systemic bone dysplasia syndrome by promoting TRAF6-induced ubiquitination degradation of YBX1 in growth plate cartilages of SMA mice. 展开更多
关键词 rna splicing hypertrophic chondrocytes Traf hypertrophic chondrocytesof SMN endochondral ossification Ybx
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Thoracic anterior controllable antedisplacement fusion for thoracic ossification of the posterior longitudinal ligament: A case report 认领 引用
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作者 Xing-Yu Jin Hua-Zheng Wang +4 位作者 Kai Yang Yu Bao Ye Wang Xing-Lei Ben Hai-Yan Sun 《World Journal of Orthopedics》 2025年第6期131-140,共10页
BACKGROUND Thoracic ossification of the posterior longitudinal ligament(T-OPLL)is caused by the ossified posterior longitudinal ligament occupying space in the spinal canal,which causes compression of the thoracic spi... BACKGROUND Thoracic ossification of the posterior longitudinal ligament(T-OPLL)is caused by the ossified posterior longitudinal ligament occupying space in the spinal canal,which causes compression of the thoracic spinal cord.Surgical treatment is difficult,risky and complicated;thus,clinical treatment is difficult at present.CASE SUMMARY A case of severe multi-segmental T-OPLL treated with thoracic anterior controllable antedisplacement fusion(TACAF)is reported,including the surgical procedures and analysis of the clinical data.The modified-Japanese Orthopaedic Association score in this patient was 4 before surgery,and it was raised to 9 after the operation.The symptoms of spinal canal compression were subsequently relieved.Three months after surgery,digital radiography showed good healing and recovery of limb sensory function.CONCLUSION This case report suggests that TACAF is feasible for the treatment of long-segment T-OPLL,and has the advantages of low risk and reduced trauma.However,this operation still needs to be verified by clinical research with a larger sample size. 展开更多
关键词 Thoracic spinal canal stenosis Ossification of posterior longitudinal ligament Spinal cord decompression Antedisplacement fusion Vertebral advancement Case report
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Vascular Ossification in the Developing Brain:A Case Study of Pediatric Sturge Weber Syndrome 认领 引用
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作者 Ranxi Chen Shuhui Xie +7 位作者 Jin Gao Shuli Zhang Xiaobin Zhang Yi Yao Gengxiu Zheng Fengpeng Wang Zili Liu Xuefeng Shen 《Neuroscience Bulletin》 SCIE CAS CSCD 2025年第3期520-524,共5页
Dear Editor,Sturge-Weber Syndrome(SWS)is a rare congenital neurocutaneous syndrome[1,2],with an estimated prevalence of 0.19 in 100,000 annually[3].It is a non-hereditary disease linked to a somatic mutation in the GN... Dear Editor,Sturge-Weber Syndrome(SWS)is a rare congenital neurocutaneous syndrome[1,2],with an estimated prevalence of 0.19 in 100,000 annually[3].It is a non-hereditary disease linked to a somatic mutation in the GNAQ,GNA11,or GNB2 gene[1],leading to vascular malformations in the cutaneous forehead,cerebral cortex,and eye[1,2].Notably,~70%of pediatric patients diagnosed with SWS exhibit brain calcification(BC)[4],though the prevalence of BC ranges from only 1%in young individuals to>20%in the senior population(>60 years old)[5].Similar to the elderly,BC in pediatric SWS patients is identified as vascular calcification[6,7],whereas BC in pediatric patients with tuberous sclerosis and tumors has been previously described as dystrophic calcification[6]. 展开更多
关键词 vascular calcification vascular malformations brain calcification bc brain calcification congenital neurocutaneous syndrome somatic mutation vascular ossification Sturge Weber syndrome
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Utility of the morphological scoring of costal cartilage ossification in age estimation of adult Egyptians using multidetector computed tomography 认领 引用
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作者 Mai Mohammad Elgendy Somaya Abdel-gawad Madkour +2 位作者 Fatma Mohamed Magdi Badr Eldine Doaa Mokhtar Emara MennattAllah Hassan Attia 《Forensic Sciences Research》 CSCD 2025年第2期75-84,共10页
Age estimation of adults is a challenging procedure in forensic practice.Inspired by the previous work by Chinese scholars,we established population-specific age estimation models from the osseous and calcified projec... Age estimation of adults is a challenging procedure in forensic practice.Inspired by the previous work by Chinese scholars,we established population-specific age estimation models from the osseous and calcified projections(OCPs)of costal cartilages,using three-dimensional volume-rendering technique.A total of 168 clinical CT scans(2 mm slice thickness)were used to develop the sex-specific age prediction models from a sample of Egyptians,comprising 70 females and 98 males,with documented ages between 12 and 85 years.The sample was also used for validating the Chinese model.We reported the differences between the predictive accuracy of the Egyptian(population specific)and Chinese(non-population specific)models.The most accurate age estimation model was stepwise linear regression with standard error of estimates of 10.9 and 11.8 years in males and females,respectively.For the simple linear regression models,the most accurate formula included OCP of the right second costal cartilage in males and OCP of the left third costal cartilage in females with standard error of estimates of 11.2 and 12.2 years,respectively,and mean absolute error(MAE)of 8.8 and 9.6 years,respectively.By comparison,the best accuracy rates produced by the Chinese vs.the Egyptian models in males and females within 5 years were 30.61%and 32.86%vs.35.71%and 32.86%,respectively,whereas within 10 years,the accuracy rates increased up to 57.14%and 58.57%vs.72.45%and 64.29%,respectively.Although the accuracy rates from the Chinese models were lower than those obtained from the Egyptian models,the MAE and least error values were comparable in both sexes.Notable accurate age estimation rates in the advanced age group≥40 years were reached being 81.25%to 97.92%in males and 69.77%to 93.02%in females.OCP of the right first costal cartilage was the most accurate in cross-population application for males and females with MAE values of 10.7 and 11.03 years,respectively,with balanced accuracy rates of age estimation using the 10-year interval and 40-year cutoff. 展开更多
关键词 forensic sciences forensic anthropology adult age estimation costal cartilage ossification linear regression cross-population validation
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Nonsurgical treatment of postoperative intestinal obstruction caused by heterotopic ossification of the mesentery:A case report 认领 引用
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作者 Jing-Tian Chen Yao-Ping Li +2 位作者 Shang-Qi Guo Jin-Sheng Huang Yong-Gang Wang 《World Journal of Gastrointestinal Surgery》 SCIE 2025年第3期385-390,共6页
BACKGROUND Among all forms of heterotopic ossification,heterotopic mesenteric ossification(HMO)is rare,with fewer than 100 reported cases to date.Postoperative early small bowel obstruction caused by HMO is even rarer... BACKGROUND Among all forms of heterotopic ossification,heterotopic mesenteric ossification(HMO)is rare,with fewer than 100 reported cases to date.Postoperative early small bowel obstruction caused by HMO is even rarer,presenting extremely high surgical risks,the potential for multiple surgeries,and a poor prognosis.There have been no reported cases of conservative treatment for resolving such early postoperative obstruction.CASE SUMMARY A 57-year-old male presented with severe postoperative small bowel obstruction shortly after undergoing open radical resection for transverse colon cancer.Laparotomy revealed extensive adhesions in the proximal jejunum and mesen-tery,making it too difficult to relieve without injuring the small bowel.Addi-tionally,multiple fixed nodules were found in the mesentery during the opera-tion.Pathology confirmed the presence of heterotopic ossification.The patient was treated with methylprednisolone on postoperative day 1,which gradually relieved his symptoms.CONCLUSION Hormone therapy may have a potential role in treating small bowel obstruction caused by early HMO after operative intervention. 展开更多
关键词 Heterotopic mesenteric ossification Hormone therapy Bowel obstruction Methylprednisolone Surgery Case report
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Targeting neutrophil extracellular traps: A novel strategy for treating heterotopic ossification 认领 引用
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作者 Chen-Yu Song Hong-Ping Yu +4 位作者 Fei-Yan Mu Jing-Shun Lu Min Yang Meng-Han Chang Kai-Yang Wang 《World Journal of Orthopedics》 2025年第11期1-6,共6页
In this article,we make a comment on the recent article by Sun et al,focusing on the advances of neutrophil extracellular traps(NETs)formation in common osteoarticular diseases.Neutrophils are the first line to elimin... In this article,we make a comment on the recent article by Sun et al,focusing on the advances of neutrophil extracellular traps(NETs)formation in common osteoarticular diseases.Neutrophils are the first line to eliminate invading pathogens including fungal and bacterial infections via releasing hydrolytic enzymes and reactive oxygen species.Besides,neutrophils will accumulate at the inflammatory site and release NETs,which are composed of histones,DNA and granular proteins.Traumatic heterotopic ossification(THO)was generally believed to develop through four stages:Inflammation,chondrogenesis,osteogenesis,and bone maturation.Thus,it can be seen that THO was related to inflammation and bone formation.Apart from immune and infectious diseases,recent studies have also shown that NETs play a significant role in the pathogenesis of THO.This article focuses on elaborating the role of NETs in the onset of THO,discussing the existing problems in the current research and outlining future directions. 展开更多
关键词 Neutrophil Neutrophil extracellular traps Heterotopic ossification Molecular mechanisms Therapeutic strategy Research progress
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When ectopic bone forms in the abdomen:The diagnostic and management challenges of heterotopic mesenteric ossification 认领 引用
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作者 Uchenna Esther Okpete Haewon Byeon 《World Journal of Gastrointestinal Endoscopy》 2025年第3期1-4,共4页
Heterotopic mesenteric ossification(HMO)is a rare medical condition,with<100 cases reported globally by 2024.This disorder is characterized by abnormal bone tissue formation within the mesentery,often following abd... Heterotopic mesenteric ossification(HMO)is a rare medical condition,with<100 cases reported globally by 2024.This disorder is characterized by abnormal bone tissue formation within the mesentery,often following abdominal trauma,ischemia,or infection.This editorial reviews the case presented by Zhang et al,involving a 34-year-old male who developed persistent left lower abdominal pain after sustaining blunt trauma to the abdomen.Diagnostic challenges arose due to the rarity and nonspecific presentation of HMO,which shares histopathological features with conditions such as myositis ossificans and necessitates differentiation from malignancies like sarcomas.Advanced imaging revealed calcifications suggestive of HMO,but definitive diagnosis was achieved only through surgical resection and histopathological analysis,which confirmed the presence of ectopic bone formation.Although benign,HMO can result in severe complications,such as bowel perforation or obstruction.Therefore,awareness of HMO is crucial for clinicians to ensure timely and appropriate treatment. 展开更多
关键词 Abdominal trauma Heterotopic mesenteric ossification Abdominal surgery Ectopic bone formation Diagnostic challenges Clinical vigilance
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The role of vascular endothelial growth factor in ossification 认领 引用 被引量：25
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作者 Yan-Qi Yang Ying-Ying Tan +3 位作者 Ricky Wong Alex Wenden Lin-Kun Zhang A bakr M Rabie 《International Journal of Oral Science》 SCIE CAS CSCD 2012年第2期64-68,共5页
Osteogenesis and angiogenesis are two closely correlated processes during bone growth, development, remodelling and repair. Vascular endothelial growth factor （VEGF） is an essential mediator during the process of an... Osteogenesis and angiogenesis are two closely correlated processes during bone growth, development, remodelling and repair. Vascular endothelial growth factor （VEGF） is an essential mediator during the process of angiogenesis. Based on an extensive literature search, which was carried out using the PubMed database and the keywords of osteogenesis, VEGF, endochondral ossification and intramembranous ossification, this manuscript reviews the role of VEGF in ossification, with emphasis on its effect in endochondral and intramembranous ossification. Osteogenesis and angiogenesis are closely correlated processes. VEGF acts as an essential mediator durin~ these processes. It not only functions in bone an^io^enesis but also in various aspects of bone develooment. 展开更多
关键词 endochondral ossification intramembranous ossification osteogenesis vascular endothelial growth factor
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Piezo1 expression in chondrocytes controls endochondral ossification and osteoarthritis development 认领 引用 被引量：21
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作者 Laura J.Brylka Assil-Ramin Alimy +18 位作者 Miriam E.A.Tschaffon-Müller Shan Jiang Tobias Malte Ballhause Anke Baranowsky Simon von Kroge Julian Delsmann Eva Pawlus Kian Eghbalian Klaus Püschel Astrid Schoppa Melanie Haffner-Luntzer David J.Beech Frank Timo Beil Michael Amling Johannes Keller Anita Ignatius Timur A.Yorgan Tim Rolvien Thorsten Schinke 《Bone Research》 SCIE CAS CSCD 2024年第1期199-214,共16页
Piezo proteins are mechanically activated ion channels,which are required for mechanosensing functions in a variety of cell types.While we and others have previously demonstrated that the expression of Piezo1 in osteo... Piezo proteins are mechanically activated ion channels,which are required for mechanosensing functions in a variety of cell types.While we and others have previously demonstrated that the expression of Piezo1 in osteoblast lineage cells is essential for boneanabolic processes,there was only suggestive evidence indicating a role of Piezo1 and/or Piezo2 in cartilage.Here we addressed the question if and how chondrocyte expression of the mechanosensitive proteins Piezo1 or Piezo2 controls physiological endochondral ossification and pathological osteoarthritis(OA)development.Mice with chondrocyte-specific inactivation of Piezo1(Piezo1Col2a1Cre),but not of Piezo2,developed a near absence of trabecular bone below the chondrogenic growth plate postnatally.Moreover,all Piezo1Col2a1Cre animals displayed multiple fractures of rib bones at 7 days of age,which were located close to the growth plates.While skeletal growth was only mildly affected in these mice,OA pathologies were markedly less pronounced compared to littermate controls at 60 weeks of age.Likewise,when OA was induced by anterior cruciate ligament transection,only the chondrocyte inactivation of Piezo1,not of Piezo2,resulted in attenuated articular cartilage degeneration.Importantly,osteophyte formation and maturation were also reduced in Piezo1Col2a1Cre mice.We further observed increased Piezo1 protein abundance in cartilaginous zones of human osteophytes.Finally,we identified Ptgs2 and Ccn2 as potentially relevant Piezo1 downstream genes in chondrocytes.Collectively,our data do not only demonstrate that Piezo1 is a critical regulator of physiological and pathological endochondral ossification processes,but also suggest that Piezo1 antagonists may be established as a novel approach to limit osteophyte formation in OA. 展开更多
关键词 Piezo1 markedly ossification
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Chondrogenesis mediates progression of ankylosing spondylitis through heterotopic ossification 认领 引用 被引量：17
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作者 Tao Yu Jianguo Zhang +13 位作者 Wei Zhu Xiao Wang Yun Bai Bin Feng Qianyu Zhuang Chang Han Shengru Wang Qimiao Hu Senbo An Mei Wan Shiwu Dong Jianzhong Xu Xisheng Weng Xu Cao 《Bone Research》 SCIE CAS CSCD 2021年第2期166-177,共12页
Ankylosing spondylitis(AS)is chronic inflammatory arthritis with a progressive fusion of axial joints.Anti-inflammatory treatments such as anti-TNF-αantibody therapy suppress inflammation but do not effectively halt ... Ankylosing spondylitis(AS)is chronic inflammatory arthritis with a progressive fusion of axial joints.Anti-inflammatory treatments such as anti-TNF-αantibody therapy suppress inflammation but do not effectively halt the progression of spine fusion in AS patients.Here we report that the autoimmune inflammation of AS generates a microenvironment that promotes chondrogenesis in spine ligaments as the process of spine fusion.Chondrocyte differentiation was observed in the ligaments of patients with earlystage AS,and cartilage formation was followed by calcification.Moreover,a large number of giant osteoclasts were found in the inflammatory environment of ligaments and on bony surfaces of calcified cartilage.Resorption activity by these giant osteoclasts generated marrow with high levels of active TGF-β,which induced new bone formation in the ligaments.Notably,no Osterix+osteoprogenitors were found in osteoclast resorption areas,indicating uncoupled bone resorption and formation.Even at the late and maturation stages,the uncoupled osteoclast resorption in bony interspinous ligament activates TGF-βto induce the progression of ossification in AS patients.Osteoclast resorption of calcified cartilage-initiated ossification in the progression of AS is a similar pathologic process of acquired heterotopic ossification(HO).Our finding of cartilage formation in the ligaments of AS patients revealed that the pathogenesis of spinal fusion is a process of HO and explained why anti-inflammatory treatments do not slow ankylosing once there is new bone formation in spinal soft tissues.Thus,inhibition of HO formation,such as osteoclast activity,cartilage formation,or TGF-βactivity could be a potential therapy for AS. 展开更多
关键词 ossification inflammation spondylitis
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Mesenchymal VEGFA induces aberrant differentiation in heterotopic ossification 认领 引用 被引量：10
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作者 Charles Hwang Simone Marini +17 位作者 Amanda KHuber David MStepien Michael Sorkin Shawn Loder Chase APagani John Li Noelle DVisser Kaetlin Vasquez Mohamed AGarada Shuli Li Jiajia Xu Ching-Yun Hsu Paul BYu Aaron WJames Yuji Mishina Shailesh Agarwal Jun Li Benjamin Levi 《Bone Research》 SCIE CAS CSCD 2019年第4期371-387,共17页
Heterotopic ossification(HO)is a debilitating condition characterized by the pathologic formation of ectopic bone.HO occurs commonly following orthopedic surgeries,burns,and neurologic injuries.While surgical excision... Heterotopic ossification(HO)is a debilitating condition characterized by the pathologic formation of ectopic bone.HO occurs commonly following orthopedic surgeries,burns,and neurologic injuries.While surgical excision may provide palliation,the procedure is often burdened with significant intra-operative blood loss due to a more robust contribution of blood supply to the pathologic bone than to native bone.Based on these clinical observations,we set out to examine the role of vascular signaling in HO.Vascular endothelial growth factor A(VEGFA)has previously been shown to be a crucial pro-angiogenic and pro-osteogenic cue during normal bone development and homeostasis.Our findings,using a validated mouse model of HO,demonstrate that HO lesions are highly vascular,and that VEGFA is critical to ectopic bone formation,despite lacking a contribution of endothelial cells within the developing anlagen. 展开更多
关键词 VEGFA injuries ossification
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High formability Mg-Zn-Gd wire facilitates ACL reconstruction via its swift degradation to accelerate intra-tunnel endochondral ossification 认领 引用 被引量：6
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作者 Xuan He Ye Li +14 位作者 Hongwei Miao Jiankun Xu Michael Tim-yun Ong Chenmin Wang Lizhen Zheng Jiali Wang Le Huang Haiyue Zu Zhi Yao Jie Mi Bingyang Dai Xu Li Patrick Shu-hang Yung Guangyin Yuan Ling Qin 《Journal of Magnesium and Alloys》 SCIE EI CAS CSCD 2024年第1期295-315,共21页
After reconstructing the anterior cruciate ligament(ACL),unsatisfactory bone tendon interface healing may often induce tunnel enlargement at the early healing stage.With good biological features and high formability,M... After reconstructing the anterior cruciate ligament(ACL),unsatisfactory bone tendon interface healing may often induce tunnel enlargement at the early healing stage.With good biological features and high formability,Magnesium-Zinc-Gadolinium(ZG21)wires are developed to bunch the tendon graft for matching the bone tunnel during transplantation.Microstructure,tensile strength,degradation,and cytotoxicity of ZG21 wire are evaluated.The rabbit model is used for assessing the biological effects of ZG21 wire by Micro-CT,histology,and mechanical test.The SEM/EDS,immunochemistry,and in vitro assessments are performed to investigate the underlying mechanism.Material tests demonstrate the high formability of ZG21 wire as surgical suture.Micro-CT shows ZG21 wire degradation accelerates tunnel bone formation,and histologically with earlier and more fibrocartilage regeneration at the healing interface.The mechanical test shows higher ultimate load in the ZG21 group.The SEM/EDS presents ZG21 wire degradation triggered calcium phosphate(Ca-P)deposition.IHC results demonstrate upregulation of Wnt3a,BMP2,and VEGF at the early phase and TGFβ3 and Type II collagen at the late phase of healing.In vitro tests also confirmed the Ca-P in the metal extract could elevate the expression of Wnt3a,βcatenin,ocn and opn to stimulate osteogenesis.Ex vivo tests of clinical samples indicated suturing with ZG21 wire did not weaken the ultimate loading of human tendon tissue.In conclusion,the ZG21 wire is feasible for tendon graft bunching.Its degradation products accelerated intra-tunnel endochondral ossification at the early healing stage and therefore enhanced bone-tendon interface healing in ACL reconstruction. 展开更多
关键词 Magnesium wire ACL reconstruction Magnesium alloy Biomaterials Endochondral ossification
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Conditional disruption of the osterix gene in chondrocytes during early postnatal growth impairs secondary ossification in the mouse tibial epiphysis 认领 引用 被引量：5
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作者 Weirong Xing Catrina Godwin +1 位作者 Sheila Pourteymoor Subburaman Mohan 《Bone Research》 SCIE CAS CSCD 2019年第3期310-317,共8页
In our previous studies, we have found that the prepubertal increase in thyroid hormone levels induces osterix(Osx) signaling in hypertrophic chondrocytes to transdifferentiate them into osteoblasts. To test if Osx ex... In our previous studies, we have found that the prepubertal increase in thyroid hormone levels induces osterix(Osx) signaling in hypertrophic chondrocytes to transdifferentiate them into osteoblasts. To test if Osx expressed in chondrocytes directly contributes to transdifferentiation and secondary ossification, we generated Osx^flox/flox;Col2-Cre-ERT2 mice and knocked out Osx with a single injection of tamoxifen at postnatal day(P) 3 prior to evaluation of the epiphyseal bone phenotype by μCT, histology, and immunohistochemistry(IHC) at P21. Vehicle(oil)-treated Osx^flox/flox;Col2-Cre-ERT2 and tamoxifen-treated, Cre-negative Osx^flox/flox mice were used as controls.μCT analysis of tibial epiphyses revealed that trabecular bone mass was reduced by 23% in the Osx conditional knockout(c KO) compared with control mice. Trabecular number and thickness were reduced by 28% and 8%,respectively, while trabecular separation was increased by 24% in the c KO mice. Trichrome staining of longitudinal sections of tibial epiphyses showed that bone area and bone area adjusted for total area were decreased by 22% and 18%, respectively. IHC studies revealed the presence of abundant Osx-expressing prehypertrophic chondrocytes in the epiphyses of control mice at P10, but not in the cKO mice. Furthermore, expression levels of MMP13, COL10, ALP, and BSP were considerably reduced in the epiphyses of cKO mice. We also found that Osx overexpression in ATDC5 chondrocytes increased expression of Col10, Mmp13, Alp, and Bsp. Our data indicate that Osx expressed in chondrocytes plays a significant role in secondary ossification by regulating expression of genes involved in chondrocyte hypertrophy and osteoblast transdifferentiation. 展开更多
关键词 ossification thyroid hormone Large chondrocyte
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Interorgan communication in neurogenic heterotopic ossification: the role of brain-derived extracellular vesicles 认领 引用 被引量：5
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作者 Weicheng Lu Jianfei Yan +11 位作者 Chenyu Wang Wenpin Qin Xiaoxiao Han Zixuan Qin Yu Wei Haoqing Xu Jialu Gao Changhe Gao Tao Ye Franklin R.Tay Lina Niu Kai Jiao 《Bone Research》 SCIE CAS CSCD 2024年第1期137-152,共16页
Brain-derived extracellular vesicles participate in interorgan communication after traumatic brain injury by transporting pathogens to initiate secondary injury.Inflammasome-related proteins encapsulated in brain-deri... Brain-derived extracellular vesicles participate in interorgan communication after traumatic brain injury by transporting pathogens to initiate secondary injury.Inflammasome-related proteins encapsulated in brain-derived extracellular vesicles can cross the blood‒brain barrier to reach distal tissues.These proteins initiate inflammatory dysfunction,such as neurogenic heterotopic ossification.This recurrent condition is highly debilitating to patients because of its relatively unknown pathogenesis and the lack of effective prophylactic intervention strategies.Accordingly,a rat model of neurogenic heterotopic ossification induced by combined traumatic brain injury and achillotenotomy was developed to address these two issues.Histological examination of the injured tendon revealed the coexistence of ectopic calcification and fibroblast pyroptosis.The relationships among brain-derived extracellular vesicles,fibroblast pyroptosis and ectopic calcification were further investigated in vitro and in vivo.Intravenous injection of the pyroptosis inhibitor Ac-YVAD-cmk reversed the development of neurogenic heterotopic ossification in vivo.The present work highlights the role of brain-derived extracellular vesicles in the pathogenesis of neurogenic heterotopic ossification and offers a potential strategy for preventing neurogenic heterotopic ossification after traumatic brain injury. 展开更多
关键词 neurogenic ossification pathogenesis
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