Finite Element Analysis of a Novel Approach for Knee and Ankle Protection during Landing

There is a high risk of serious injury to the lower extremities during a human drop landing. Prophylactic knee and ankle braces are commonly used to reduce injury by restraining the motion of joints. However, braces that restrain joint range of motion (ROM) may have detrimental effects on the user’s kinematical performance and joint function. The present study aimed to propose a novel set of double-joint braces and to evaluate its protective performance in terms of the ankle and knee. Accordingly, the finite element method was performed to investigate the biomechanical responses of the ankle and knee in braced and unbraced conditions. The results showed that the semi-rigid support at the ankle joint can share the high impact force that would otherwise be inflicted on one’s lower extremity, thereby reducing the peak stress on the inferior articular surface of the tibia, menisci, and articular cartilages, as well as the horizontal force on the talus. Moreover, with knee bending, the elongated spring component at the knee joint can convert the impact kinetic energy into elastic potential energy of the spring; meanwhile, the retractive force generated by the spring also provides a more balanced interaction between the menisci and articular cartilages. This biomechanical analysis can accordingly provide inspiration for new approaches to place human lower extremities at lower risk during landings.

Repairing effects of glucosamine sulfate in combination with etoricoxib on articular cartilages of patients with knee osteoarthritis

Purpose: To evaluate the repairing effects of glucosamine sulfate combined with etoricoxib on articular cartilages of patients with knee osteoarthritis (KOA). Methods: A total of 106 KOA patients were randomly divided into control (n=40) and experimental groups (n=66), and treated with etoricoxib alone and glucosamine sulfate plus etoricoxib respectively. Changes in WOMAC score and clinical efficacy were observed. The synovial fluid was extracted. Bone metabolism indices, growth factors, inflammatory factors, matrix metalloproteinases (MMPs) and NO-induced apoptosis-related factors were measured by ELISA. JNK and Wnt5a mRNA levels were determined using RT-PCR. Results: After treatment, the total WOMAC scores of both groups significantly declined (P<0.05), being lower in experimental group. The total effective rate of experimental group was higher (P<0.05). BGP and OPG levels rose, especially in experimental group (P<0.05). CTX-II, COMP and RANKL levels decreased, particularly in experimental group (P<0.05). TGF-β, IGF-1 and FGF-2 levels increased, especially in experimental group (P<0.05). Both groups, particularly experimental group, had decreased levels of IL-1β, IL-17, IL-18, TNF-α, MMP-3, MMP-9 and MMP-13 (P<0.05). JNK and Wnt5a mRNA levels of both groups dropped, which were lower in experimental group (P<0.05). NO and LPO levels reduced, being lower in experimental group. SOD level rose, especially in experimental group (P<0.05). Conclusion: Glucosamine sulfate plus etoricoxib can repair the articular cartilages of KOA patients. Probably, JNK and Wnt5a are down-regulated to inhibit the secretion of MMPs through lowering the levels of inflammatory factors, thereby delaying cartilage matrix degradation. NO-induced chondrocyte apoptosis may be suppressed via the SOD pathway.

Repairing effects of glucosamine sulfate in combination with etoricoxib on articular cartilages of patients with knee osteoarthritis

Purpose: To evaluate the repairing effects of glucosamine sulfate combined with etoricoxib on articular cartilages of patients with knee osteoarthritis (KOA). Methods: A total of 106 KOA patients were randomly divided into control (n=40) and experimental groups (n=66), and treated with etoricoxib alone and glucosamine sulfate plus etoricoxib respectively. Changes in WOMAC score and clinical efficacy were observed. The synovial fluid was extracted. Bone metabolism indices, growth factors, inflammatory factors, matrix metalloproteinases (MMPs) and NO-induced apoptosis-related factors were measured by ELISA. JNK and Wnt5a mRNA levels were determined using RT-PCR. Results: After treatment, the total WOMAC scores of both groups significantly declined (P<0.05), being lower in experimental group. The total effective rate of experimental group was higher (P<0.05). BGP and OPG levels rose, especially in experimental group (P<0.05). CTX-II, COMP and RANKL levels decreased, particularly in experimental group (P<0.05). TGF-β, IGF-1 and FGF-2 levels increased, especially in experimental group (P<0.05). Both groups, particularly experimental group, had decreased levels of IL-1β, IL-17, IL-18, TNF-α, MMP-3, MMP-9 and MMP-13 (P<0.05). JNK and Wnt5a mRNA levels of both groups dropped, which were lower in experimental group (P<0.05). NO and LPO levels reduced, being lower in experimental group. SOD level rose, especially in experimental group (P<0.05). Conclusion: Glucosamine sulfate plus etoricoxib can repair the articular cartilages of KOA patients. Probably, JNK and Wnt5a are down-regulated to inhibit the secretion of MMPs through lowering the levels of inflammatory factors, thereby delaying cartilage matrix degradation. NO-induced chondrocyte apoptosis may be suppressed via the SOD pathway.

Biological Potential Alterations of Migratory Chondrogenic Progenitor Cells during Knee Osteoarthritic Progression

Background: Although increasing studies have demonstrated that chondrogenic progenitor cells (CPCs) remain present in human osteoarthritic cartilage, the biological alterations of the CPCs from the less diseased lateral tibial condyle and the more diseased medial condyle of same patient remain to be investigated. Methods: CPCs were isolated from paired grade 1-2 and grade 3-4 osteoarthritic cartilage by virtue of cell migratory capacities. The cell morphology, immunophenotype, self-renewal, multi-differentiation, and cell migration of these CPCs were evaluated. Additionally, the distributions of CD105+/CD271+ cells in OA osteochondral specimen were determined. Furthermore, a high-through mRNA sequencing was performed. Results: Migratory CPCs (mCPCs) robustly outgrew from mildly collagenases-digested osteoarthritic cartilages. The mCPCs from grade 3-4 cartilages (mCPCs, grade 3-4) harbored morphological characteristics, cell proliferation and colony formation capacity that were similar to those of the mCPCs from the grade 1-2 OA cartilages (mCPCs, grade 1-2). However, the mCPCs (grade 3-4) highly expressed CD271. In addition, the mCPCs (grade 3-4) showed enhanced osteo-adipogenic activities and decreased chondrogenic capacity. Furthermore, the mCPCs (grade 3-4) exhibited stronger cell migration in response to osteoarthritis synovial fluids. More CD105+/CD271+ cells resided in grade 3-4 articular cartilages. Moreover, the results of mRNA sequencing showed that mCPCs (grade 3-4) expressed higher migratory molecules. Conclusions: Our data suggest that more mCPCs (grade 3-4) migrate to injured articular cartilages but with enhanced osteo-adipogenic and decreased chondrogenic capacity, which might explain the pathological changes of mCPCs during the progression of OA from early to late stages. Thus, these dysfunctional mCPCs might be optional cell targets for OA therapies.

Biological Potential Alterations of Migratory Chondrogenic Progenitor Cells during Knee Osteoarthritic Progression

Background: Although studies have demonstrated that chondrogenic progenitor cells (CPCs) remain present in human osteoarthritic cartilage, the heterogeneity of CPCs subpopulations, the biological alterations of CPCs, and their contributions to the progression of osteoarthritis remain to be investigated. Methods: CPCs were isolated from paired grade 1-2 and grade 3-4 osteoarthritic cartilage by virtue of cell migratory capacities. The cell morphology, immunophenotype, self-renewal, multidifferentiation, and cell migration of these CPCs were evaluated. Additionally, the distributions of CPCs in articular cartilage were determined by immuno-histochemical staining. Furthermore, a high-through mRNA sequencing was performed to explore the underlying mechanisms. Results: Migratory CPCs (mCPCs) robustly outgrew from collagenases-digested osteoarthritic cartilages for 2 weeks after the initial culture. The mCPCs from grade 3-4 cartilages (mCPCs, grade 3-4) harbored morphological characteristics, cell proliferation and colony formation capacity that were similar to those of the mCPCs from the grade 1-2 cartilages (mCPCs, grade 1-2). However, the mCPCs (grade 3-4) highly expressed CD271. In addition, the mCPCs (grade 3-4) showed enhanced osteo-adipogenic activities and decreased chondrogenic capacity. Furthermore, the mCPCs (grade 3-4) exhibited stronger cell migration in response to osteoarthritis synovial fluids. More CD105+ cells resided in grade 3-4 superficial articular cartilages. Moreover, the results of mRNA sequencing showed that mCPCs (grade 3-4) expressed higher migratory molecules. Conclusions: Our data suggest that more mCPCs (grade 3-4) migrate to injured articular cartilages but with decreased cartilage-repairing capacity, which might accelerate cartilage degradation. Thus, these dysfunctional mCPCs might be a novel cell target to alleviate cartilage lesions.

Experimental Study on Creep Characteristics of Microdefect Articular Cartilages in the Damaged Early Stage

Traumatic joint injury is known to cause cartilage deterioration and osteoarthritis. In order to study the mechanical mechanism of damage evolution on articular cartilage, taking the fresh porcine articular cartilage as the experimental samples, the creep experiments of the intact cartilages and the cartilages with different depth defect were carried out by using the noncontact digital image correlation technology. And then, the creep constitutive equations of cartilages were established. The results showed that the creep curves of different layers changed exponentially and were not coincident for the cartilage sample. The defect affected the strain values of the creep curves. The creep behavior of cartilage was dependent on defect depth. The deeper the defect was, the larger the strain value was. The built three-parameter viscoelastic constitutive equation had a good correlation with the experimental results and could predict the creep performance of the articular cartilage. The creep values of the microdefective cartilage in the damaged early stage were different from the diseased articular cartilage. These findings pointed out that defect could accelerate the damage of cartilage. It was helpful to study the mechanical mechanism of damage evolution.

Finite Element Modelling Simulated Meniscus Translocation and Deformation during Locomotion of the Equine Stifle

We developed a finite element model (FEM) of the equine stifle joint to identify pressure peaks and simulate translocation and deformation of the menisci. A series of sectional magnetic resonance images (1.5 T) of the stifle joint of a 23 year old Shetland pony gelding served as basis for image segmentation. Based on the 3D polygon models of femur, tibia, articular cartilages, menisci, collateral ligaments and the meniscotibial ligaments, an FEM model was generated. Tissue material properties were assigned based on data from human (Open knee(s) project) and bovine femoro-tibial joint available in the literature. The FEM model was tested across a range of motion of approximately 30°. Pressure load was overall higher in the lateral meniscus than in the medial. Accordingly, the simulation showed higher translocation and deformation in the lateral compared to the medial meniscus. The results encourage further refinement of this model for studying loading patterns on menisci and articular cartilages as well as the resulting mechanical stress in the subchondral bone (femur and tibia). A functional FEM model can not only help identify segments in the stifle which are predisposed to injury, but also to better understand the progression of certain stifle disorders, simulate treatment/surgery effects and to optimize implant/transplant properties.