Osteoarthritis and rheumatoid arthritis are the most ubiquitous joint disorders which cause tremendous loss of life quality and impose an economic burden on society. At present, the treatment options for these two diseases comprise non-operative and surgical treatments, amongst those total knee arthroplasties (TKA). Various studies have recognized smoking as a significant risk factor for postoperative complications. Therefore, the purpose of this study was to examine the impact of smoking on the incidence and postoperative complications after a total knee arthroplasty by a systematic review and meta-analysis. The research was performed using PUBMED, Cochrane Library and EMBASE, extracting data from thirteen suitable studies and incorporating 2,109,482 patients. Cohort studies evaluating the impact of smoking on TKA with sufficient data were included for the study, and cohort studies without a proper control group and complete data were excluded. A fixed-effects or random-effects model was used to measure the pooled risk ratio (RR) or hazard ratio (HR) with 95% confidence interval (CI). Compared to non-smokers, smokers had a significantly lower incidence of TKA (p<0.01). However, smokers had a higher incidence of total complications (p=0.01), surgical complications (p<0.01), pneumonia (p<0.01) and revision surgery (p=0.01). No significant difference in the risk of blood transfusion (p=0.42), deep vein thrombosis (p=0.31), pulmonary embolism (p=0.34), urinary tract infection (p=0.46) or mortality (p=0.39) was found between smokers and non-smokers. In conclusion, the study indicated that tobacco has two diametrically opposite effects on TKA patients: 1. Tobacco increases the incidence of surgical complications, pneumonia and revision after TKA; 2. It decreases the overall risk of being a candidate for TKA.

This study aimed to quantitatively analyze subchondral vascularization during the progression of osteoarthritis (OA) in the elderly, particularly regarding the timing of initial blood vessel emergence and when their density peaks. A total of 129 independent areas from 43 human femoral heads, obtained through arthroplasty for OA or hemiarthroplasty for fractures, were analyzed. The femoral heads were grouped by Kellgren-Lawrence (KL) grades: KL 1 (6 heads), KL 2 (14 heads), KL 3 (10 heads), and KL 4 (13 heads), and the Mankin score was assessed. Quantitative measurements of blood vessel length 1 mm below the tidemark, cartilage volume and thickness, chondrocyte volume, ECM volume, subchondral bone volume, and bone marrow volume were performed using stereology and immunohistochemistry. The most substantial increase in the characteristics of blood vessels within the subchondral region began at KL 3 and peaked at KL 4. Blood vessel volume increased from 6.71 ± 5.84 mm ³ in group KL 1 to 156.21 ± 138.67 mm ³ in group KL 4 ( p < 0.001). Blood vessel surface area showed an increase from 14.78 ± 9.89 cm ² (group KL 1) to 125.20 ± 93.18 cm ² (group KL 4) ( p < 0.001). Likewise, blood vessel length grew from 27.53 m (IQR 13.70–65.41 m) in group KL 1 to 112.03 ± 76.07 m in group KL 4 ( p = 0.001). This study offers deeper insights into the role of vascularization in OA pathophysiology, quantifying subchondral blood vessel characteristics in the femoral head across different OA stages.

Objective: To explore the relationship between cerebrospinal fluid-contacting neurons (CSF-cNs) and endogenous neural progenitor cells (ENPCs) and whether CSF-cNs are involved in nerve repair after spinal cord injury (SCI). Methods: Cholera toxin B-horseradish peroxidase complex (CB-HRP) and cholera toxin B conjugated with saporin (CB-SAP) were injected into the lateral ventricles of spinal cord injured rats to mark and destroy the CSF-cNs. Then the rats in the experimental group were injured by SCI. Observe the content and co-expression of CSF-cNs and ENPCs in rats of each group, and observe the recovery of motor function after SCI in each group. Results: After the destruction of CSF-cNs, the number of ENPCs decreased significantly in the long term after the surgery, and the recovery of motor function also deteriorated as compared to the group with intact CSF-cNs. Meanwhile some cells in the spinal cord express both the biological marker of CSF-cNs and ENPCs. Conclusion: This study shows that the population of ENPCs and motor function recovery in SCI rats declined after the destruction of CSF-cNs, suggesting that CSF-cNs affect the ENPCs population and may be involved in the recovery of neural function after SCI.

Osteosarcoma is a primary malignant bone tumor with no effective treatment. Apoptosis, one of the programmed cell death, is any pathological form of cell death mediated by intracellular processes. Under the pathological state, the unregulated regulation of apoptosis can disrupt the balance between cell proliferation and death, causing osteosarcoma proliferation and metastasis. As carcinogenic or tumor suppressor factors, microRNAs (miRNAs) regulate apoptosis of osteosarcoma cells by regulating apoptosis-related signaling pathways and apoptosis-related genes. This review provides the current knowledge of miRNAs and their target genes related to the apoptosis of osteosarcoma.