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 summarize the effect of cartilage progenitor cells (CPCs) and microRNA-140 (miR-140) on the repair of osteoarthritic cartilage injury, and analyze their clinical prospects. Methods The recent researches regarding the CPCs, miR-140, and repair of cartilage in osteoarthritis (OA) disease were extensively reviewed and summarized. Results CPCs possess the characteristics of self-proliferation, expression of stem cell markers, and multi-lineage differentiation potential, and their chondrogenic ability is superior to other tissues-derived mesenchymal stem cells. CPCs are closely related to the development of OA, but the autonomic activation and chondrogenic ability of CPCs around the osteoarthritic cartilage lesion cannot meet the requirements of complete cartilage repair. miR-140 specifically express in cartilage, and has the potential to activate CPCs by inhibiting key molecules of Notch signaling pathway and enhance its chondrogenic ability, thus promoting the repair of osteoarthritic cartilage injury. Intra-articular delivery of drugs is one of the main methods of OA treatment, although intra-articular injection of miR-140 has a significant inhibitory effect on cartilage degeneration in rats, it also exhibit some limitations such as non-targeted aggregation, low bioavailability, and rapid clearance. So it is a good application prospect to construct a carrier with good safety, cartilage targeting, and high-efficiency for miR-140 based on articular cartilage characteristics. In addition, CPCs are mainly dispersed in the cartilage surface, while OA cartilage injury also begins from this layer, it is therefore essential to emphasize early intervention of OA. Conclusion miR-140 has the potential to activate CPCs and promote the repair of cartilage injury in early OA, and it is of great clinical significance to further explore the role of miR-140 in OA etiology and to develop new OA treatment strategies based on miR-140.
Osteoporosis is a degenerative disease characterized by decreased bone mass and destruction of bone microstructure. At present, previous studies have found that the structure and content of type Ⅰ collagen fibers are closely related to osteoporosis. However, there have been few studies on the prevention and treatment of osteoporosis using type Ⅰ collagen fibers as therapeutic targets. In this paper, the relationships between type Ⅰ collagen fibers and osteoporosis, biomechanics, bone matrix and bone strength are discussed. At the same time, the regulation of type Ⅰ collagen-related signaling pathways in osteoporosis is summarized, such as the signaling pathways of cathepsin K, transforming growth factor-β/Sma- and Mad-related protein, transforming growth factor-β/bone morphogenetic protein, c-jun N-terminal protein kinase and Wnt/β-catenin, in order to provide a new therapeutic direction for the prevention and treatment of osteoporosis.
ObjectiveTo summarize research progress of change in bone mineral density (BMD) after knee arthroplasty and its diagnostic methods, influencing factors, and drug prevention and treatment.MethodsThe relevant literature at home and abroad was reviewed and summarized from research status of the advantages and disadvantages of BMD assessment methods, the trend of changes in BMD after knee arthroplasty and its influencing factors, and the differences in effectiveness of drugs.ResultsThe central BMD and mean BMD around the prosthesis decrease after knee arthroplasty, which is closely associated with body position, age, weight, daily activities, and the fixation methods, design, and material of prosthesis. Denosumab, bisphosphonates, and teriparatide et al. can decrease BMD loss after knee arthroplasty.ConclusionBMD after knee arthroplasty decreases, which is related to various factors, but the mechanism is unclear. At present, some inhibitors of bone resorption can decrease BMD loss after knee arthroplasty. However, its long-term efficacy remains to be further explored.
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.