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.
Objective To summarize the role of chondrocytes mitochondrial biogenesis in the pathogenesis of osteoarthritis (OA), and analyze the applications in the treatment of OA. Methods A review of recent literature was conducted to summarize the changes in mitochondrial biogenesis in the course of OA, the role of major signaling molecules in OA chondrocytes, and the prospects for OA therapeutic applications. Results Recent studies reveales that mitochondria are significant energy metabolic centers in chondrocytes and its dysfunction has been considered as an essential mechanism in the pathogenesis of OA. Mitochondrial biogenesis is one of the key processes maintaining the normal quantity and function of mitochondria, and peroxisome proliferator-activated receptor-gamma coactivator 1 alpha (PGC-1α) is the central regulator of this process. A regulatory network of mitochondrial biogenesis with PGC-1α as the center, adenosine monophosphate-activated protein kinase, sirtuin1/3, and cyclic adenosine monophosphate response element-binding protein as the main upstream regulatory molecules, and nuclear respiratory factor 1, estrogen-related receptor α, and nuclear respiratory factor 2 as the main downstream regulatory molecules has been reported. However, the role of mitochondrial biogenesis in OA chondrocytes still needs further validation and in-depth exploration. It has been demonstrated that substances such as puerarin and omentin-1 can retard the development of OA by activating the damaged mitochondrial biogenesis in OA chondrocytes, which proves the potential to be used in the treatment OA. ConclusionMitochondrial biogenesis in chondrocytes plays an important role in the pathogenesis of OA, and further exploring the related mechanisms is of great clinical significance.
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.
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.
Objective To compare differences in the cl inical outcomes between percutaneous pinning with plaster spl int and open reduction and pull ing out wire in the treatment of mallet fingers. Methods From December 2002 to September 2007, 72 patients with mallet fingers were treated. They were divided into two groups: group A and group B. In group A, 38 patients were treated by open reduction and pull ing out wire, 34 males and 4 females, aged (26.0 ± 8.5) years. Among them, 2 patients were injured in the index finger, 11 in the middle finger, 18 in the ring finger and 7 in the l ittle finger. Thirtythreepatients suffered from sports injuries, 5 from fall ing wounds. The average time between the injury and the surgery was(6.1 ± 3.1) days. In group B, 34 patients were treated by percutaneous pinning with plaster spl int, 26 males and 8 females, aged (28.1 ± 10.7) years. Among them, 1 patient was injured in the index finger, 9 in the middle finger, 15 in the ring finger and 9 in the l ittle finger. Thirty-one patients suffered from sports injuries, 3 from fall ing wounds. The average time between the injury and the surgery was (6.3 ± 3.6) days. All the fingers had typical mallet malformation, and X-ray films showed avulsed fractures of distal-segment phalanxes at the dorsal basilar part. Results The operation time was (61.8 ± 12.8) minutes in group A and (7.0 ± 2.6) minutes in group B. All patients in both groups were followed up for 6-24 months (11.9 months on average in group A and 13.2 months in group B). In group A, apart from 3 patients who had flap necrosis and infection, all the other patients obtained heal ing by first intention. One patient had palmar skin ulcer at 6 days after the operation and healed after proper treatment. Thirty-six patients gained bone union at (47.6 ± 8.7) days postoperatively and 2 patients had pseudarthrosis, which improved after reconstruction of the extensor tendon attachment point. According to the total active movement (TAM) functional assessment system, 10 cases were e cellent, 18 good, 8 fair and 2 poor, with the choiceness rate of 73.7%. In group B, all incisions obtained heal ing by first intention without pin-track infection, flap necrosis and migration of the pins and gained bone union at (27.7 ± 3.9) days after the operation. According to the TAM functional assessment system, 19 cases were excellent, 13 good and 2 fair, with the choiceness rate of 94.1%. There were significant differences between the two groups in operation time, compl ications, heal ing time and choiceness rate (P lt; 0.05). Conclusion Percutaneous pinning with plaster spl int is simple in operation and has smaller incisions and fewer compl ications compared with open reduction and pull ing out wire, andproves to be a useful way in the treatment of mallet fingers.
ObjectiveTo review the research progress on finite element analysis (FEA) of unicompartmental knee arthroplasty (UKA) in medial knee compartmental osteoarthritis.MethodsThe FEA research literature on the medial knee UKA at home and abroad was reviewed, and the progress on the aspects of the influences of the prosthesis arrangement and the postoperative joint line on the mechanical distribution of the knee joint, the improvement of the UKA prosthesis, and the related research of different types of prostheses were summarized.ResultsAt present, scholars have conducted a large number of FEA studies on UKA in the medial knee compartmental osteoarthritis. The results of the study show that the recommended coronal alignment and the tibial slope angle of tibial component in medial fixed-bearing UKA are 0° and 5°-7°, respectively; and the coronal alignment and the tibial slope angle of tibial component in mobile-bearing UKA are 4° varus to 4° valgus and 5°-7°, respectively. The femoral component is arranged in the neutral position of the distal femur. The joint line is recommended to be the primary alignment. The anatomical UKA prosthesis can restore the biomechanical properties of the normal knee joint.ConclusionFEA research can clarify the best arrangement and joint line of the medial knee UKA prosthesis based on the mechanical distribution results, and guide the design of UKA prostheses that are more suitable for patients.