Acute septic arthritis is on the rise among all patients. Acute septic arthritis must be extensively assessed, identified, and treated to prevent fatal consequences. Antimicrobial therapy administered intravenously has long been considered the gold standard for treating acute osteoarticular infections. According to clinical research, parenteral antibiotics for a few days, followed by oral antibiotics, are safe and effective for treating infections without complications. This article focuses on bringing physicians up-to-date on the most recent findings and discussions about the epidemiology, etiology, diagnosis, and treatment of acute septic arthritis. In recent years, the emergence of antibiotic-resistant, particularly aggressive bacterial species has highlighted the need for more research to enhance treatment approaches and develop innovative diagnosis methods and drugs that might combat better in all patients. This article aims to furnish radiologists, orthopaedic surgeons, and other medical practitioners with contemporary insights on the subject matter and foster collaborative efforts to improve patient outcomes. This review represents the initial comprehensive update encompassing patients across all age groups.

Osteoarthritis (OA) is the most prevalent joint disease characterized by degradation of articular cartilage, inflammation, and changes in periarticular and subchondral bone of joints. Osteoporosis (OP) is another systemic skeletal disease characterized by low bone mass and bone mineral density (BMD) accompanied by microarchitectural deterioration in bone tissue and increased bone fragility and fracture risk. Both OA and OP are mainly affected on the elderly people. Recent studies have shown that osteopontin (OPN) plays a vital role in bone metabolism and homeostasis. OPN involves these biological activities through participating in the proliferation, migration, differentiation, and adhesion of several bone-related cells, including chondrocytes, synoviocytes, osteoclasts, osteoblasts, and marrow mesenchymal stem cells (MSCs). OPN has been demonstrated to be closely related to the occurrence and development of many bone-related diseases, such as OA and OP. This review summarizes the role of OPN in regulating inflammation activity and bone metabolism in OA and OP. Furthermore, some drugs that targeted OPN to treat OA and OP are also summarized in the review. However, the complex mechanism of OPN in regulating OA and OP is not fully elucidated, which drives us to explore the depth effect of OPN on these two bone diseases.

Background: To investigate whether osteopontin (OPN) affects autophagy in human osteoarthritic chondrocytes and determine the roles of CD44, αvβ3 integrin and the Mitogen-activated protein kinase (MAPK) pathway in this progress.Methods: First, we compared the autophagy levels in the human osteoarthritis (OA) and normal cartilage, then, we cultured human OA chondrocytes in vitro and treated cells with recombinant human OPN (rhOPN) to determine autophagy changes. Next, the anti-CD44 and anti-CD51/61 monoclonal antibodies (Abs) or isotype IgG were used to determine the possible role of CD44 and αvβ3 integrin; subsequently, an inhibitor of the ERK MAPK pathway was used to investigate the role of ERK MAPK. Western blotting was used to measure the Beclin1, LC3 II and MAPK proteins expressions, mRFP-GFP-LC3 confocal imaging and transmission electron microscopy were also used to detect the autophagy levels. Cell Counting Kit-8 (CCK-8) was used to assay the proliferation and activity of chondrocytes.Results: The LC3 protein was greatly decreased in OA cartilage compared to normal cartilage, and OPN suppressed the autophagy activity in chondrocytes in vitro. Blocking experiments with anti-CD44 and anti-CD51/61 Abs indicated that OPN could suppress the expression of LC3II and Beclin1 through αvβ3 integrin and CD44. Our results also indicated that the ratio of p-ERK/ERK but not p-P38/P38 and p-JNK/JNK was increased after the rhOPN treatment. The ERK inhibitor inhibited the activity of OPN in the suppression of autophagy, and the CCK-8 results showed that rhOPN could promote chondrocyte proliferation.Conclusion: OPN inhibited chondrocyte autophagy through CD44 and αvβ3 integrin receptors and via the ERK MAPK signaling pathway.

Arthritis is the most prevalent joint disease and is characterized by articular cartilage degradation, synovial inflammation, and changes in periarticular and subchondral bone. Recent studies have reported that Yes-associated protein (YAP) and the transcriptional coactivator with PDZ-binding motif (TAZ) have significant effects on the proliferation, migration, and survival of chondrocytes and fibroblast-like synovial cells (FLSs). YAP/TAZ signaling pathway, as well as the related Hippo–YAP signaling pathway, are responsible for the condition of cells and articular cartilage in joints. They are tightly regulated to maintain metabolism in chondrocytes and FLSs because abnormal expression may result in cartilage damage. However, the roles and mechanisms of the Hippo–YAP pathway in arthritis remain largely unknown. This review summarizes the roles and key functions of YAP/TAZ and the Hippo–YAP signaling pathway in FLSs and chondrocytes for the induction of proliferation, migration, survival, and differentiation in rheumatoid arthritis (RA) and osteoarthritis (OA) research. We also discuss the therapeutic strategies involving YAP/TAZ and the related Hippo-YAP signaling pathway involved in OA.

Sepsis-related mortality rates are high among elderly patients, especially those in intensive care units (ICUs). Early prediction of the prognosis of sepsis is critical, as prompt and effective treatment can improve prognosis. Researchers have predicted mortality and the development of sepsis using machine learning algorithms; however, few studies specifically focus on elderly patients with sepsis. This paper proposes a viable model for early prediction of in-hospital mortality among elderly patients diagnosed with sepsis. We extracted patient information from the Medical Information Mart for Intensive Care IV database. We employed several machine learning algorithms to predict the in-hospital mortality of elderly ICU patients with sepsis. The performance of the model was evaluated by using the AUROC and score. Furthermore, the SHAP algorithm was used to explain the model, analyze how the individual features affect the model output, and visualize the Shapley value for a single individual. Our study included 18522 elderly patients, with a mortality of 15.4%. After screening, 59 clinical variables were extracted to develop models. Feature importance analysis showed that age, PO2, RDW, SPO2, WBC, and urine output were significantly related to the in-hospital mortality. According to the results of AUROC (0.871 (95% CI: 0.854–0.888)) and score (0.547 (95% CI: 0.539–0.661)) analyses, the extreme gradient boosting (XGBoost) model outperformed the other models (i.e., LGBM, LR, RF, DT, and KNN). Furthermore, SHAP force analysis illustrated how the constructed model visualized the individualized prediction of death. XGBoost machine learning framework gives good in-hospital mortality prediction of elderly patients with sepsis and can maximize prediction model accuracy. The XGBoost model could be an effective tool to assist doctors in identifying high-risk cases of in-hospital mortality among elderly patients with sepsis. This could be used to create a clinical decision support system in the future.

Background: Cartilage destruction is the main characteristic of osteoarthritis (OA), and osteopontin (OPN) is elevated in OA articular cartilage; however, the reason for the increased OPN level is not determined. In addition, Wnt/β-catenin signaling participates in the progression of OA. The aim of the present study was to evaluate whether canonical Wnt signaling could regulate the expression of OPN in human chondrocytes in vitro. Methods: Human chondrocytes were cultured in vitro, and we first assayed the mRNA levels of OPN and β-catenin in chondrocytes. Next, we performed transient transfection of TCF 4 shRNA into chondrocytes to inhibit TCF 4 expression and explore changes in the OPN level. Then, the Wnt/β-catenin signaling inhibitor Dickkopf-1 (Dkk-1) was incubated with chondrocytes, and we assayed the changes in β-catenin and OPN. Results: Our results showed that the expression of both β-catenin and OPN was increased in OA chondrocytes, but there were no correlations between β-catenin and OPN expression. TCF4 shRNA downregulated the expression of TCF 4 and OPN in chondrocytes, while after treatment with rDKK-1 at a concentration of 400 ng/ml for 24 h, the mRNA and protein expression of both β-catenin and OPN was significantly decreased in chondrocytes. Conclusions: Elevated OPN expression might be regulated by the β-catenin/TCF-4 pathway, and the Wnt/β-catenin inhibitor DKK1 could inhibit the expression of β-catenin and OPN in OA chondrocytes.