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Osteoarthritis (OA) is the most common joint disease worldwide and a leading cause of disability. Characterized by degradation of articular cartilage, synovial inflammation, and changes in periarticular and subchondral bone, OA can negatively impact an individual's physical and mental well-being. Recent studies have reported several critical signaling pathways as key regulators and activators of cellular and molecular processes during OA development. Wnt signaling is one such pathway whose signaling molecules and regulators were shown to be abnormally activated or suppressed. As such, agonists and antagonists of those molecules are potential candidates for OA treatment. Notably, a recent phase I clinical trial (NCT02095548) demonstrated the potential of SM04690, a small-molecule inhibitor of the Wnt signaling pathway, as a disease-modifying oseoarthritis drug (DMOAD). This review summarizes the role and mechanism of Wnt signaling and related molecules in regulating OA progression, with a view to accelerating the translation of such evidence into the development of strategies for OA treatment, particularly with respect to potential applications of molecules targeting the Wnt signaling pathway.

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Comparative studies have been carried out among solid-state chitosan soliquoid, chitosan acetic acid physiological saline solution, and carboxymethyl chitosan physiological saline solution to discover the hemostatic effect of molecular weight (M(w)) and deacetylation degree (DA) of chitosan. It was found that solid-state chitosan and chitosan acetic acid physiological saline solution performed different hemostatic mechanisms. When blood mixed with chitosan acetic acid physiological saline solution, the erythrocytes aggregated and were deformed. The DA, especially a low DA, in the chitosan acetic acid physiological saline solution, had a significant effect on the unusual aggregation and deformation of erythrocytes, compared with the effect of M(w) within a range between 10(5) and 10(6). However, this phenomenon could not be observed in solid-state chitosan soliquoid. Solid-state chitosan with a low DA absorbed more platelets and was more hemostatic. Carboxymethyl chitosan physiological saline solution had nothing to do with the aggregation and deformation of erythrocytes but caused local rouleau. The values of thrombin time (TT), prothrombin time (PT), activated partial thromboplastin time (APTT), and fibrinogen concentration (FIB) were measured after the blood was mixed with solid-state chitosan soliquoid, chitosan acetic acid physiological saline solution, and carboxymethyl chitosan physiological saline solution, separately. The results demonstrated that coagulation factors might not be activated by them.