Objective To introduce the research progress on the relationship between gut microbiota dysbiosis and osteoarthritis (OA), focus on the possible mechanism of gut microbiota dysbiosis promoting OA, and propose a new therapeutic direction. Methods The domestic and foreign research literature on the relationship between gut microbiota dysbiosis and OA was reviewed. The role of the former in the occurrence and development of OA and the new ideas for the treatment of OA were summarized. Results The gut microbiota dysbiosis promotes the development of OA mainly in three aspects. First, the gut microbiota dysbiosis destroys intestinal permeability and causes low-grade inflammation, which aggravate OA. Secondly, the gut microbiota dysbiosis promotes the development of OA through metabolic syndrome. Thirdly, the gut microbiota dysbiosis is involved in the development of OA by regulating the metabolism and transport of trace elements. Studies have shown that improving gut microbiota dysbiosis by taking probiotics and transplanting fecal microbiota can reduce systemic inflammation and regulate metabolic balance, thus treating OA. Conclusion Gut microbiota dysbiosis is closely related to the development of OA, and improving gut microbiota dysbiosis can be an important idea for OA treatment.
Objective To introduce the characteristics of tetrahedral framework nucleic acids (tFNA), focusing on its application in the treatment of osteoarthritis (OA) and relationship with microRNA (miRNA), and prospect the application of tFNA in the treatment of OA and the new idea of constructing miR-tFNA functional complex to treat OA. Methods Recent studies were extensively reviewed to analyze the mechanism of tFNA and its relationship with OA and miRNA. Results tFNA, a new type of new carrier, can not only play an indirect role in the treatment of OA as a small molecular carrier with therapeutic effect, but also play a direct role through the regulation of chondrocytes. It can bind with the miRNA that can regulate OA. The therapeutic effect of constructing tFNA functional complex loaded with miRNA has been verified in various diseases, and tFNA has advantages compared with other vectors. Conclusion tFNA, a novel framework nucleic acid structure, plays an important role in the treatment of OA. Constructing miR-tFNA functional complex may be an innovative idea in the treatment of OA.
Objective To summarize the research progress of bioactive scaffolds in the repair and regeneration of osteoporotic bone defects. Methods Recent literature on bioactive scaffolds for the repair of osteoporotic bone defects was reviewed to summarize various types of bioactive scaffolds and their associated repair methods. Results The application of bioactive scaffolds provides a new idea for the repair and regeneration of osteoporotic bone defects. For example, calcium phosphate ceramics scaffolds, hydrogel scaffolds, three-dimensional (3D)-printed biological scaffolds, metal scaffolds, as well as polymer material scaffolds and bone organoids, have all demonstrated good bone repair-promoting effects. However, in the pathological bone microenvironment of osteoporosis, the function of single-material scaffolds to promote bone regeneration is insufficient. Therefore, the design of bioactive scaffolds must consider multiple factors, including material biocompatibility, mechanical properties, bioactivity, bone conductivity, and osteogenic induction. Furthermore, physical and chemical surface modifications, along with advanced biotechnological approaches, can help to improve the osteogenic microenvironment and promote the differentiation of bone cells. ConclusionWith advancements in technology, the synergistic application of 3D bioprinting, bone organoids technologies, and advanced biotechnologies holds promise for providing more efficient bioactive scaffolds for the repair and regeneration of osteoporotic bone defects.
ObjectiveTo investigate biomechanical effects of pseudo-patella baja on stress of patellofemoral joint after total knee arthroplasty (TKA) by using finite element analysis (FEA).MethodsA series of CT and MRI of the left knee joint of two healthy volunteers and three-dimensional (3D) scanned data of TKA prosthesis were taken, and the 3D models of knee before and after TKA were established. The finite element model of pseudo-patella baja, normal patella, and alta patella after TKA were constructed by Insall-Salvafi (IS) ratio and Blackburne-Peel (BP) ratio. The load was applied along the direction of quadriceps femoris. After testing the validity of the finite element model, the high contact stress of patellofemoral joint was measured on the von Mise stress nephogram of pseudo-patella baja, normal patella, and alta patella after TKA when the knee flexion was 30°, 60°, and 90°. The average contact area was calculated according to two volunteers’ data.ResultsOn the finite element model of the normal patella after TKA with knee flexion 30°, 475 N pressure was applied along the direction of quadriceps femoris. The contact stress of patellofemoral joint was (1.29±0.41) MPa, which was similar to the results reported previously. The finite element model was valid. The von Mise stress nephogram showed that the stress mainly focused on the medial patellofemoral articular surface during knee flexion, and the contact point gradually moved up with the knee flexion deepened. The stress on the medial and lateral patellofemoral articular surface increased with the knee flexion deepened but decreased with the increase of patellar height. The effects of patellar height and knee flexion on the high contact stress of patellofemoral joint were similar among the finite element models after TKA based on the data of two volunteers. The high contact stress of patellofemoral joint increased with the knee flexion deepened in the same patellar height models (P<0.05), but decreased with the increase of patellar height in the same knee flexion models (P<0.05). The high contact stress of patellofemoral joint of pseudo-patella baja model was significantly higher than normal and alta patella models (P<0.05). The average contact area of patellofemoral joint of pseudo-patella baja was bigger than normal and alta patella models with the knee flexion deepened.ConclusionThe pseudo-patella baja after TKA has an important effect on the biomechanics of patellofemoral joint. Reserving the joint line and avoiding the occurrence of pseudo-patella baja can decrease the risk of anterior knee pain, patellar arthritis, and other complications caused by the increasing of contact stress of patellofemoral joint.
ObjectiveTo summarize the role of chondrocyte mitochondrial homeostasis imbalance in the pathogenesis of osteoarthritis (OA) and analyze its application prospects. Methods The recent literature at home and abroad was reviewed to summarize the mechanism of mitochondrial homeostasis imbalance, the relationship between mitochondrial homeostasis imbalance and the pathogenesis of OA, and the application prospect in the treatment of OA. Results Recent studies have shown that mitochondrial homeostasis imbalance, which is caused by abnormal mitochondrial biogenesis, the imbalance of mitochondrial redox, the imbalance of mitochondrial dynamics, and damaged mitochondrial autophagy of chondrocytes, plays an important role in the pathogenesis of OA. Abnormal mitochondrial biogenesis can accelerate the catabolic reaction of OA chondrocytes and aggravate cartilage damage. The imbalance of mitochondrial redox can lead to the accumulation of reactive oxygen species (ROS), inhibit the synthesis of extracellular matrix, induce ferroptosis and eventually leads to cartilage degradation. The imbalance of mitochondrial dynamics can lead to mitochondrial DNA mutation, decreased adenosine triphosphate production, ROS accumulation, and accelerated apoptosis of chondrocytes. When mitochondrial autophagy is damaged, dysfunctional mitochondria cannot be cleared in time, leading to ROS accumulation, which leads to chondrocyte apoptosis. It has been found that substances such as puerarin, safflower yellow, and astaxanthin can inhibit the development of OA by regulating mitochondrial homeostasis, which proves the potential to be used in the treatment of OA. Conclusion The mitochondrial homeostasis imbalance in chondrocytes is one of the most important pathogeneses of OA, and further exploration of the mechanisms of mitochondrial homeostasis imbalance is of great significance for the prevention and treatment of OA.