Ilizarov technique for treating elbow stiffness caused by myositis ossificans: A case report.

BACKGROUND: Myositis ossificans (MO) is a rare disease involving the formation of bone outside the musculoskeletal system. While surgical intervention is the main treatment approach, preventing recurrence and standardized rehabilitation are also crucial. Here, we present a surgical strategy to prevent the recurrence of MO. CASE SUMMARY: A 28-year-old female patient was admitted for the first time for a comminuted fracture of the left olecranon. However, incorrect postoperative rehabilitation resulted in the development of elbow joint stiffness with ectopic ossification, causing a loss of normal range of motion. The patient was diagnosed with MO based on physical examination, X-ray findings, and clinical presentation. We devised a surgical strategy to remove MO, followed by fixation with an Ilizarov frame, and implemented a scientifically reasonable rehabilitation plan. The surgery lasted for 3 h with an estimated blood loss of 45 mL. A drainage tube was placed after surgery, and fluid was aspirated through ultrasound-guided puncture. The patient experienced a significant reduction in joint stiffness after surgery. In the final follow-up at 9 mouths, there was evident improvement in the range of motion of the elbow joint, and no other symptoms were reported. CONCLUSION: The Ilizarov frame is an advantageous surgical technique for facilitating rehabilitation after MO removal. It offers benefits such as passive recovery, individualized treatment, and prompt recovery.

Corrigendum: Single-cell RNA sequencing reveals the difference in human normal and degenerative nucleus pulposus tissue profiles and cellular interactions.

[This corrects the article DOI: 10.3389/fcell.2022.910626.].

Single-cell RNA landscape of osteoimmune microenvironment in osteoporotic vertebral compression fracture and Kümmell's disease.

Background: Single-cell RNA sequencing (scRNA-seq) enables specific analysis of cell populations at single-cell resolution; however, there is still a lack of single-cell-level studies to characterize the dynamic and complex interactions between osteoporotic vertebral compression fractures (OVCFs) and Kümmell's disease (KD) in the osteoimmune microenvironment. In this study, we used scRNA-seq analysis to investigate the osteoimmune microenvironment and cellular composition in OVCFs and KD. Methods: ScRNA-seq was used to perform analysis of fractured vertebral bone tissues from one OVCF and one KD patients, and a total of 8,741 single cells were captured for single-cell transcriptomic analysis. The cellularity of human vertebral bone tissue was further analyzed using uniform manifold approximation and projection. Pseudo-time analysis and gene enrichment analysis revealed the biological function of cell fate and its counterparts. CellphoneDB was used to identify the interactions between bone cells and immune cells in the osteoimmune microenvironment of human vertebral bone tissue and their potential functions. Results: A cellular profile of the osteoimmune microenvironment of human vertebral bone tissue was established, including mesenchymal stem cells (MSCs), pericytes, myofibroblasts, fibroblasts, chondrocytes, endothelial cells (ECs), granulocytes, monocytes, T cells, B cells, plasma cells, mast cells, and early erythrocytes. MSCs play an immunoregulatory function and mediate osteogenic differentiation and cell proliferation. The differentiation trajectory of osteoclasts in human vertebral bone tissue was also revealed. In addition, ECs actively participate in inflammatory infiltration and coupling with bone cells. T and B cells actively participate in regulating bone homeostasis. Finally, by identifying the interaction of ligand-receptor pairs, we found that immune cells and osteoclasts have bidirectional regulatory characteristics, have the effects of regulating bone resorption by osteoclasts and promoting bone formation, and are essential for bone homeostasis. It is also highlighted that CD8-TEM cells and osteoclasts might crosstalk via CD160-TNFRSF14 ligand-receptor interaction. Conclusion: Our analysis reveals a differential landscape of molecular pathways, population composition, and cell-cell interactions during OVCF development into KD. OVCFs exhibit a higher osteogenic differentiation capacity, owing to abundant immune cells. Conversely, KD results in greater bone resorption than bone formation due to depletion of MSCs and a relatively suppressed immune system, and this immune imbalance eventually leads to vertebral avascular necrosis. The site of action between immune cells and osteoclasts is expected to be a new therapeutic target, and these results may accelerate mechanistic and functional studies of osteoimmune cell types and specific gene action in vertebral avascular necrosis and pathological bone loss diseases, paving the way for drug discovery.

Corrigendum: Single-cell RNA sequencing reveals the difference in human normal and degenerative nucleus pulposus tissue profiles and cellular interactions.

[This corrects the article DOI: 10.3389/fcell.2022.910626.].

Single-Cell RNA Sequencing Reveals the Difference in Human Normal and Degenerative Nucleus Pulposus Tissue Profiles and Cellular Interactions.

Background: The nucleus pulposus is a constituent structure of the human intervertebral disc, and its degeneration can cause intervertebral disc degeneration (IDD). However, the cellular and molecular mechanisms involved remain elusive. Methods: Through bioinformatics analysis, the single-cell transcriptome sequencing expression profiles of human normal nucleus pulposus (NNP) cells and human degenerative nucleus pulposus (DNP) cells were compared to clarify the transcriptome differential expression profiles of human NNP and DNP. The single-cell sequencing results of the two samples were analyzed using bioinformatics methods to compare the differences in histiocytosis between human NNP and DNP, map the histiocytes of NNP and DNP, perform cell differentiation trajectories for the cell populations of interest and predict cell function, and explore their heterogeneity by pathway analysis and Gene Ontology analysis. Results: Nine cell types were identified, which were chondrocyte 1, chondrocyte 2, chondrocyte 3, chondrocyte 4, chondrocyte 5, endothelial, macrophage, neutrophil, and T cells. Analysis of the proportion of chondrocytes in different tissues revealed that chondrocyte 1 accounted for a higher proportion of NNP cells and highly expressed COL2A1 compared with DNP cells; chondrocyte 2, chondrocyte 3, chondrocyte 4, and chondrocyte 5 accounted for a higher proportion of DNP cells compared with NNP cells. Among them, chondrocyte 2 was an inhibitory calcified chondrocyte with high expression of MGP, chondrocytes 3 were fibrochondrocytes with high expression of COL1A1, chondrocytes 4 were chondrocytes that highly express pain inflammatory genes such as PTGES, and chondrocytes 5 were calcified chondrocytes with high expression of FN1 (chondrocytes 4 and chondrocytes 5 were found for the first time in a study of single-cell transcriptome sequencing of disc tissue). Cell trajectory analysis revealed that chondrocyte 1 was at the beginning of the trajectory and chondrocyte 3 was at the end of the trajectory, while chondrocyte 5 appeared first in the trajectory relative to chondrocyte 2 and chondrocyte 4. Conclusion: After functional identification of the specifically expressed genes in five chondrocytes, it was found that chondrocyte 1 was a chondrocyte with high expression of COL2A1, COL9A2, COL11A2, and CHRDL2 in a high proportion of NNP cells, and chondrocyte 3 was a fibrochondrocyte with high expression of COL1A1, COL6A3, COL1A2, COL3A1, AQP1, and COL15A1 in an increased proportion during nucleus pulposus cell degeneration. Through cell trajectory analysis, it was found that chondrocytes 5 specifically expressing FN1, SESN2, and GDF15 may be the key cells leading to degeneration of nucleus pulposus cells. Chondrocytes 2 expressing MGP, MT1G, and GPX3 may play a role in reversing calcification and degeneration, and chondrocytes 4 expressing PTGES, TREM1, and TIMP1 may play a role in disc degeneration pain and inflammation.

Columbianetin alleviates lipopolysaccharides (LPS)-induced inflammation and apoptosis in chondrocyte through activation of autophagy by inhibiting serum and glucocorticoid-induced protein kinase 1 (SGK1) expression.

Osteoarthritis (OA) is a degenerative disease of articular cartilage involving the entire joint tissue. Columbianetin (CBT) is a major active compound of radix angelicae pubescentis, which is used in the treatment of OA. This paper attempts to explore the role of CBT in OA. Lipopolysaccharides (LPS) was used to induce mouse chondrocytes ATDC5. The effect of CBT on cell viability in ATDC5 cells with or without LPS induction was determined by CCK-8 and LDH kits. The inflammatory response was evaluated using ELISA kits. Apoptosis in LPS-induced ATDC5 cells were examined by TUNEL staining. The expression of apoptosis and autophagy-related proteins was tested with Western blot. The relationship between CBT and serum and glucocorticoid-induced protein kinase 1 (SGK1) was examined by RT-qPCR, Western blot, and molecular docking. After SGK1 overexpression or addition of the autophagy inhibitor 3-methyladenine (3 MA), the above experiments were done again. Results revealed that CBT increased LPS-induced decrease in ATDC5 cell viability. CBT inhibited inflammation triggered by LPS, evidenced by reduced levels of TNF-α, IL-6 and IL-1ß. Cell apoptosis was attenuated following CBT adding in ATDC5 cells exposed to LPS, accompanied by upregulated Bcl-2 expression and downregulated Bax and cleaved caspase 3 expression. In addition, CBT elevated Beclin1 and LC3II/LC3I expression but decreased p62 expression. Additionally, CBT inhibited SGK1 expression. However, SGK1 overexpression or 3 MA reversed the effects of CBT on LPS-induced loss of ATDC5 cell viability, inflammation, apoptosis and autophagy. Collectively, CBT could improve OA through the activation of chondrocyte autophagy by suppressing SGK1 expression.

A Prediction Model of the Concrete Cracking Induced by the Non-Uniform Corrosion of the Steel Reinforcement.

This paper investigates the influence of non-uniform corrosion in the transversal direction of the steel reinforcement on the cracking propagation of the concrete cover. An analytical model is proposed for the prediction of the corrosion-induced cracking performance. Both the thick cylinder theory of the concrete and the effect of transversal non-uniform corrosion of the steel reinforcement are involved by considering the corrosion layer of the corrosion products and a layer of concrete with the corrosion products filled with the pores. A three-stage corrosion-induced cracking of the concrete is proposed: corrosion without expansive stress to the concrete, corrosion with expansive stress to the adjacent concrete, as well as the corrosion-induced cracking of the concrete. By considering the non-uniform corrosion of the steel reinforcement and the tensile stress induced by the volumetric expansion of the corrosion products, the cracking initiation resulting from the non-uniform corrosion was involved in the prediction model. The models were also validated by the experimental results from both the corroded specimens and the existing literature, which would be helpful for the evaluation of the existing reinforced concrete constructions in the marine environment.