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.

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 polysaccharide from Fagopyrum esculentum Moench bee pollen alleviates microbiota dysbiosis to improve intestinal barrier function in antibiotic-treated mice.

Antibiotics are the most commonly used clinical drugs for anti-infection, but they can also destroy normal microorganisms and cause intestinal barrier dysfunction. To elucidate the effects and mechanism of a water-soluble polysaccharide from Fagopyrum esculentum Moench bee pollen (WFPP) on intestinal barrier integrity in antibiotic-treated mice, BALB/c mice were exposed to a broad-spectrum antibiotic (ceftriaxone) or not (control), and were administered low-, medium- and high-dose WFFP (100 mg kg-1, 200 mg kg-1 and 400 mg kg-1, respectively) daily by oral gavage for 3 weeks. Mice treated with ceftriaxone displayed symptoms of growth retardation, atrophy of immune organs including thymus and spleen, increased gut permeability, and intestinal barrier damage, which were restored after intervention with WFFP at different doses. Moreover, the beneficial effects of WFFP were closely associated with enhanced intestinal sIgA secretion and reduced inflammatory response. Furthermore 16S rDNA gene sequencing revealed that WFPP elevated microbial diversity and richness and changed the community structure, therefore, alleviating microbiota dysbiosis caused by ceftriaxone. Interestingly, WFPP could modulate the abundance of sIgA secretion-related bacteria (e.g. Proteobacteria) and inflammation-related bacteria (e.g. Enterococcus). Therefore, WFPP can relieve antibiotic-induced microbiota dysbiosis to improve intestinal barrier integrity by increasing intestinal sIgA secretion and inhibiting inflammation.