[Incidence of blood transfusion and associated risk factors during hip arthroplasty hospitalization].

OBJECTIVE: To investigate the incidence and risk factors of blood transfusion during hospitalization in patients receiving hip arthroplasty. METHODS: Clinical data of 347 hip arthroplasty patients admitted between January and January 2019 and December 2021. Patients were divided into 184 patients in the transfusion group and 164 patients in the nontransfusion group according to whether they received blood transfusion during hospitalization. The basic medical history data, biochemical results and surgical conditions of the patients in two groups were collected and compared. They were divided into total hip arthroplasty (THA) and hemiarthroplasty (HA) according to the different surgical methods. One-way analysis and Spearman correlation were used to analyze the factors associated with blood transfusion in hip arthroplasty patients. Multi-factor logistic regression analysis was performed for statistically significant(P<0.05) indicators, thus screening for independent risk factors for blood transfusion during hospitalization in hip arthroplasty patients. The receiver operating characteristic(ROC)curves for intraoperative bleeding in all hip arthroplasty patients, total hip arthroplasty patients, and hemi arthroplasty patients were plotted and compared, and area under curve(AUC) and the optimal threshold were calculated. RESULTS: A total of 347 patients were included for hip arthroplasty, including 207 total hip arthroplasty and 140 hemi arthroplasty. The transfusion rates of all hip arthroplasty patients, total hip arthroplasty patients and hemi arthroplasty patients were 53.03%(184/347), 53.14%(110/207) and 52.86%(74/140), respectively. Multifactorial logistic regression analysis showed that preoperative cystatin C (OR=2.739, P=0.001), hemoglobin at admission (OR=0.960, P<0.000 1), intraoperative bleeding (OR=1.010, P<0.000 1), postoperative pneumonia (OR=1.897, P=0.024), and right hip arthroplasty (OR=2.277, P=0.002) were independent risk factors for all hip arthroplasty patients;hemoglobin at admission (OR=0.978, P=0.016), intraoperative bleeding (OR=1.012, P<0.000 1), and postoperative pneumonia (OR=2.769, P=0.013) were independent risk factors for total hip arthroplasty;hemoglobin at admission (OR=0.930, P<0.000 1), intraoperative bleeding (OR=1.010, P<0.000 1), preoperative cystatin C (OR=2.277, P=0.023), and right hip arthroplasty (OR=2.428, P=0.046) were independent risk factors for hemi arthroplasty. Hemoglobin on admission and intraoperative bleeding were common risk factors for total and hemi arthroplasty. The AUCs were 0.688, 0.778, and 0.652 for total hip arthroplasty patients, total hip arthroplasty patients, and hemi arthroplasty patients, respectively. CONCLUSION: Intraoperative bleeding volume and preoperative hemoglobin are important risk factors for transfusion during hip arthroplasty hospitalization, and cystatin C may be a new biomarker for transfusion during hip arthroplasty hospitalization. At the same time, given the high incidence and potential risk of blood transfusion in hip arthroplasty, interventions should be made during hospitalization for identified risk factors.

[Progress of intraosseous basivertebral nerve ablation for symptomatic Modic alterations].

Chronic lumbar and back pain caused by degenerative vertebral endplates presents a challenging issue for patients and clinicians. As a new minimally invasive spinal treatment method, radiofrequency ablation of vertebral basal nerve in bone can denature the corresponding vertebral basal nerve through radiofrequency ablation of degenerative vertebral endplate. It blocks the nociceptive signal transmission of the vertebral base nerve, thereby alleviating the symptoms of low back pain caused by the degenerative vertebral endplate. At present, many foreign articles have reported the operation principle, operation method, clinical efficacy and related complications of radiofrequency ablation of the vertebral basal nerve. The main purpose of this paper is to conduct a comprehensive analysis of the current relevant research, and provide a reference for the follow-up clinical research.

Trim21 depletion alleviates bone loss in osteoporosis via activation of YAP1/ß-catenin signaling.

Despite the diverse roles of tripartite motif (Trim)-containing proteins in the regulation of autophagy, the innate immune response, and cell differentiation, their roles in skeletal diseases are largely unknown. We recently demonstrated that Trim21 plays a crucial role in regulating osteoblast (OB) differentiation in osteosarcoma. However, how Trim21 contributes to skeletal degenerative disorders, including osteoporosis, remains unknown. First, human and mouse bone specimens were evaluated, and the results showed that Trim21 expression was significantly elevated in bone tissues obtained from osteoporosis patients. Next, we found that global knockout of the Trim21 gene (KO, Trim21-/-) resulted in higher bone mass compared to that of the control littermates. We further demonstrated that loss of Trim21 promoted bone formation by enhancing the osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs) and elevating the activity of OBs; moreover, Trim21 depletion suppressed osteoclast (OC) formation of RAW264.7 cells. In addition, the differentiation of OCs from bone marrow-derived macrophages (BMMs) isolated from Trim21-/- and Ctsk-cre; Trim21f/f mice was largely compromised compared to that of the littermate control mice. Mechanistically, YAP1/ß-catenin signaling was identified and demonstrated to be required for the Trim21-mediated osteogenic differentiation of BMSCs. More importantly, the loss of Trim21 prevented ovariectomy (OVX)- and lipopolysaccharide (LPS)-induced bone loss in vivo by orchestrating the coupling of OBs and OCs through YAP1 signaling. Our current study demonstrated that Trim21 is crucial for regulating OB-mediated bone formation and OC-mediated bone resorption, thereby providing a basis for exploring Trim21 as a novel dual-targeting approach for treating osteoporosis and pathological bone loss.

Elevated expression of ICAM-1 in synovium is associated with early inflammatory response for cartilage degeneration in type 2 diabetes mellitus.

Type 2 diabetes mellitus (T2DM) is increasingly being recognized as an independent risk factor for the onset and progression of osteoarthritis (OA). Extensive studies have focused on the contribution of obesity (excessive mechanical stress), comorbidity frequently found in T2DM, to cartilage destruction during OA development. However, a little is known about how diabetes-related inflammation may affect the local cartilage in a diabetic objective. In the present study, we were able to establish a T2DM rat model using a combination of a low dose of streptozotocin with high-fat and high-sugar diet. Although the cartilage integrity was comparable between the control and T2DM groups, the expression of matrix metalloproteinases-13 (MMP-13) was significantly upregulated in T2DM, indicating the initiation of an early cascade of cartilage degeneration. In parallel, an obvious alteration of subchondral bone remodeling (inhibition of bone formation) was observed, as evidenced by the reduction of osterix-expressing positive cells. Moreover, we demonstrated that the expression of intercellular adhesion molecule-1 (ICAM-1) in the serum and synovium of T2DM rats was elevated, accompanied by an increase of synovitis score. We also noticed that the number of F4/80-positive macrophage cells was significantly increased in the T2DM group. Mechanistically, the expression of ICAM-1 in fibroblast-like synoviocytes can be triggered by glucose and interleukin-1ß, which are the two important factors within the joint of T2DM. Given that MMP-13 expression was significantly upregulated in the T2DM cartilage, and that ICAM-1-mediated filtration of macrophage was associated with synovitis, we propose that ICAM-1 is essential for triggering a vicious cycle of inflammation within the joint, which together subsequently drivers the cartilage degradation.

CD54+ rabbit adipose-derived stem cells overexpressing HIF-1α facilitate vascularized fat flap regeneration.

Fat flap transplantation is frequently performed in patients suffering from soft tissue defects resulting from disease or trauma. This study explored the feasibility of constructing vascularized fat flaps using rabbit adipose-derived stem cells (rASCs) and collagen scaffolds in a rabbit model. We evaluated rASCs proliferation, paracrine function, adipogenesis, vascularization, and CD54 expression, with or without HIF-1α transfection in vitro and in vivo. We observed that adipogenic differentiation potential was greater in rASCs with high CD54 expression (CD54+rASCs) than in those with low expression (CD54-rASCs), both in vitro and in vivo. HIF-1α overexpression not only augmented this effect, but also enhanced cell proliferation and paracrine function in vitro. We also demonstrated that HIF-1α-transfected CD54+rASCs showed enhanced paracrine function and adipogenic capacity, and that paracrine function increases expression of angiogenesis-related markers. Thus, CD54+rASCs overexpressing HIF-1α enhanced large volume vascularized fat flap regeneration in rabbits, suggesting CD54 may be an ideal candidate marker for ASCs adipogenic differentiation.