RationaleChondrosarcoma is a malignant mesenchymal tumor originating from cartilage. The pelvis, ribs, femur, and humerus are the most frequently affected sites, and scapula involvement is relatively rare. The aim of the present study was to report a case of chondrosarcoma in the scapula.Patient concernsA 42-year-old woman presented with a 3-month history of a painful mass in the right scapula.Diagnoses and interventionThe patient underwent tumor resection. The post-operative pathological diagnosis was scapula chondrosarcoma.OutcomesFollowing resection, the patient continued to receive routine follow-up care. There was no recurrence or tumor metastasis at a follow-up of 5 years.ConclusionsSurgery remains the primary therapy for chondrosarcoma. One of the greatest challenges in the management of chondrosarcoma is to accurately assess tumor grade before surgical intervention. Chemotherapy and radiotherapy have been applied without success. Chemo- and radioresistance have been examined beyond classic phenotypic properties to identify more efficient therapeutic strategies. Therefore, development of future novel therapies is contingent upon elucidating the molecular mechanisms of chondrosarcoma.
Osteoporosis (OP) is a common bone metabolic disease, the process of which is fundamentally irreversible. Therefore, the investigation into osteoblastic differentiation of bone marrow mesenchymal stem cells (BMSCs) will provide more clues for OP treatment. In the present study, we found that microRNA-187-5p (miR-187-5p) played a key role on osteoblastic differentiation, which was significantly upregulated during osteogenic differentiation of BMSCs in mice. Moreover, overexpression of miR-187-5p suppressed osteoblastic differentiation of BMSCs through increasing alkaline phosphatase (ALP), matrix mineralization, and levels of Osterix (OSX), and osteopontin (OPN) as well as runt-related transcription factor 2 (Runx2) in vitro. The results in vivo indicated that the upregulation of miR-187-5p enhanced the efficacy of new bone formation in the heterotopic bone formation assay. Luciferase reporter assay and western blot analysis revealed that miR-187-5p was involved in osteogenesis by targeting intracellular adhesion molecule 1 (ICAM-1). Furthermore, ICAM-1 silence inhibited osteoblastic differentiation of BMSCs. Taken together, our results suggested for the first time that miR-187-5p may promote osteogenesis by targeting ICAM-1, and provided a possible therapeutic target for bone metabolic diseases.
Recent studies have shown that the differentiation of bone marrow mesenchymal stem cells (BMSCs) into osteogenic lineages can promotes bone formation and maintains bone homeostasis, which has become a promising therapeutic strategy for skeletal diseases such as osteoporosis. Fructus Ligustri Lucidi (FLL) has been widely used for the treatment of osteoporosis and other orthopedic diseases for thousands of years. However, whether FLL plays an anti-osteoporosis role in promoting the osteogenic differentiation of BMSCs, as well as its active components, targets, and specific molecular mechanisms, has not been fully elucidated. First, we obtained 13 active ingredients of FLL from the Traditional Chinese Medicine Systems Pharmacology (TCSMP) database, and four active ingredients without any target were excluded. Subsequently, 102 common drug-disease targets were subjected to protein-protein interaction (PPI) analysis, Gene Oncology (GO), and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses. The results of the three analyses were highly consistent, indicating that FLL promoted the osteogenic differentiation of BMSCs by activating the PI3K/AKT signaling pathway. Finally, we validated previous predictions using in vitro experiments, such as alkaline phosphatase (ALP) staining, alizarin red staining (ARS), and western blot analysis of osteogenic-related proteins. The organic combination of network pharmacological predictions with in vitro experimental validation comprehensively confirmed the reliability of FLL in promoting osteogenic differentiation of BMSCs. This study provides a strong theoretical support for the specific molecular mechanism and clinical application of FLL in the treatment of bone formation deficiency.
Regulation of mitochondrial metabolism is becoming an important target in inhibiting necrosis and apoptosis following secondary spinal cord injury, and physiological compounds that reduce mitochondrial dysfunction are regarded as efficient protective reagents following injury. It has been demonstrated that spermine, a polyamine composed of four primary amines, may be taken up by a mitochondria‑specific uniporter and may preserve mitochondrial bioenergetics, suggesting that it may be important in the pathophysiology of mitochondria. However, the protective mechanism has not yet been definitively clarified. In the present study, isolated spinal cord mitochondria were incubated with spermine to evaluate its physiological functions and Src kinase activities. The results revealed that spermine increased oxidative phosphorylation, attenuated mitochondrial swelling and maintained the membrane potential. An inhibitor of Src kinases, amino‑5-(4‑chlorophenyl)‑7‑(t‑butyl)pyrazolo[3,4‑d]pyrimidine (PP2), markedly reduced the effects of spermine. However, inhibition of tyrosine phosphatases by vanadate led to marginal increases in the effects of spermine. Therefore, the present study hypothesized that tyrosine phosphorylation sites are present in the subunits of respiratory chains and mitochondrial permeability transition pore proteins, which may be modified via phosphorylation and dephosphorylation. Furthermore, spermine may upregulate the phosphorylation of Src kinases, and PP2 and vanadate conversely regulate Src phosphorylation. The results of the present study suggest that spermine is a strategic regulator within mitochondria that may activate Src kinases in the spinal cord, and tyrosine phosphorylation signaling is a primary regulatory pathway of mitochondrial metabolism.
Silicon-substituted calcium phosphate (Si-CaP) is a promising bioactive material for bone tissue engineering. The mechanism of Si-CaP regulates osteogenic-angiogenic coupling during bone regeneration has not been fully elucidated. In this study, we screened the targets of Si-CaP and osteogenic-angiogenic coupling. 83 common genes were regarded as key targets for Si-CaP regulation of the osteogenic-angiogenic coupling. Then, we performed protein-protein interaction analysis, GO and KEGG enrichment analysis of these 83 targets to further predict their molecular mechanism. Our results showed that Si-CaP treatment could regulate the osteogenic-angiogenic coupling by up-regulating the expression of Toll-like receptor 4 (TLR4), and the phosphorylation of AKT which in turn activating the PI3K/AKT signaling pathway, promoting the expression of RUNX2, OPN, VEGF. In addition, we also found that TLR4 siRNA treatment could block the PI3K/AKT signaling pathway, while inhibiting the promoting effect of Si-CaP. However, although LY294002 can achieve the same inhibitory effect as TLR4 siRNA by blocking the PI3K/AKT signaling pathway, it could not affect the expression of TLR4. This indicates that TLR4 is an upstream activator of PI3K/AKT signaling pathway. These results are highly consistent with the prediction of bioinformatics. In conclusion, we have elucidated the role of TLR4/PI3K/AKT signaling axis in Si-CaP mediated osteogenic-angiogenic coupling for the first time. This study provides new data onto the regulatory role and molecular mechanism of Si-CaP in the process of osteogenic-angiogenic coupling, which strongly supports its wide application for bone tissue engineering.
Rationale:Desmoplastic fibroma (DF) is a rare, locally invasive but benign bone tumor. It represents one of the rarest bone diseases, with an incidence of only 0.11% of all primary bone tumors.Patient concerns:Herein, a case of massive and unusual DF, with simultaneous involvement of ilium and ischium, is described. A 29-year-old man suffered minor pain in his right hip for 2 years. It worsened after sudden movements, which prevented him from walking normally. Physical examination showed a limitation when the right hip was flexed and a percussion pain on the hip region. A medical imaging examination showed that the right ilium and ischium had a massive bone lesion. The top of acetabular had very little bone left and a fracture was likely at any time. No prominent body weight loss was noted, because there was no extensive invasion to the adjacent soft tissue.Diagnoses:DF of the Ilium and Ischium.Interventions:The patient underwent a surgery involving curettage and grafting to maintain the stability of the pelvis.Outcomes:The definitive pathological diagnosis was DF, without evidence of malignancy. The postoperative recovery course at 3-month follow-up was uneventful.Lessons:To the authors’ knowledge, such a massive DF involving both ilium and ischium has been rarely reported. Young patients require appropriate and timely treatment modalities.
Prosthesis loosening after THA is a rather common complication. For DDH patients with Crowe IV, the surgical risk and complexity is significant. THA with S-ROM prosthesis combined with subtrochanteric osteotomy is a common treatment. However, loosening of a modular femoral prosthesis (S-rom) is uncommon in THA and has a very low incidence. With modular prostheses distal prosthesis looseness are rarely reported. Non-union osteotomy is a common complication of subtrochanteric osteotomy. We report three patients with Crowe IV DDH who developed prosthesis loosening following THA with an S-ROM prosthesis and subtrochanteric osteotomy. We addressed the management of these patients and prosthesis loosening as likely underlying causes.
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