Why incongruous knee replacements do not fail early

Rapid failure of knee prostheses does not usually occur, despite the non-conforming nature of the articulation between femoral and tibial components and the associated large contact pressures. This theoretical study examines the likelihood of fatigue fracture of a layered elastic model loaded by a sliding cylindrical indenter. Cracks (line-defects) were assumed to have nucleated within the layer. The stress intensity factors (SIFs) associated with these cracks were calculated. The values obtained for the SIFs are quite low, with a corresponding low likelihood of crack-growth. When taken in conjunction with the experimentally derived fatigue laws of previous investigators, they suggest that short line-cracks should not grow. It seems that early failures have not simply been due to large shear stresses which occur beneath the prosthesis surface. Other factors, such as the degradation of material through heat-pressing, sterilisation or oxidation, or the deleterious effect of fusion defects, may be required to drive the cracks to delamination.     

Dominant role of interface over knee angle for cushioning impact loading and regulating initial leg stiffness

For in vivo impact loadings administered under controlled initial conditions, it was hypothesized that larger initial knee angles (IKA) and softer impacting interfaces would reduce impact loading and initial leg stiffness. A human pendulum was used to deliver controlled impacts to the right foot of 21 subjects for three IKA (0, 20 and 40°) and three interfaces (barefoot, soft and hard EVA foams). The external impact force and the shock experienced by the subjects' shank were measured simultaneously with a wall mounted force platform and a skin mounted accelerometer, respectively. Stiffness of the leg was derived using impact velocity and wall reaction force data. The results disproved the role of the knee joint in regulating initial leg stiffness and provided only partial support for the hypothesized improved cushioning. Larger knee flexion at contact reduced impact force but increased the shock travelling throughout the shank. Conversely, softer interfaces produced sizable reductions in both initial leg stiffness and severity of the impact experienced by the lower limb. Force rate of loading was found to be highly correlated (r=0.95) to limb stiffness that was defined by the heel fat pad and interface deformations. These results would suggest that interface interventions are more likely to protect the locomotor system against impact loading than knee angle strategies.     

Faster intrinsic rate of torque development in elbow flexors than knee extensors: Effect of muscle architecture?

We studied the effect of pennate vs. fusiform muscle architecture on the rate of torque development (RTD) by examining the predominately fusiform elbow flexors (EF) and highly-pennate knee extensors (KE). Seventeen male volunteers (28.4 ± 6.2 years) performed explosive isometric EF and KE contractions (MVCs). Biceps brachii and vastus lateralis fascicle angles were measured to confirm their architecture, and both the rate of voluntary muscle activation (root-mean-square EMG in the 50 ms before contraction onset; EMG_-50) and electromechanical delay (EMD; depicting muscle-tendon series elasticity) were assessed as control variables to account for their influence on RTD. MVC torque, early (RTD₅₀) and late (RTD₂₀₀) RTDs were calculated and expressed as absolute and normalized values. Absolute MVC torque (+412%), RTD₅₀ (+215%), and RTD₂₀₀ (+427%) were significantly (p < 0.001) higher in KE than EF. However, EF RTD₅₀ was faster (+178%) than KE after normalization (p = 0.02). EMG_-50 and EMD did not differ between muscle groups. The results suggest that the faster absolute RTD in KE is largely associated with its higher maximal torque capacity, however in the absence of differences in rates of muscle activation, fiber type, and EMD the fusiform architecture of EF may be considered a factor allowing its faster early RTD relative to strength capacity.     

METTL3-mediated m6A modification of IGFBP7-OT promotes osteoarthritis progression by regulating the DNMT1/DNMT3a-IGFBP7 axis

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Reduction in range of movement can increase maximum voluntary eccentric forces for the human knee extensor muscles

Using the KinCom 500H isokinetic dynamometer the first part of this study measured the characteristics of the force velocity relationship curve for the human knee extensors between -1.57 (eccentric) and 3.67 (concentric) rads x s(-1) (-90 and 210 degrees s(1)) for both legs in 4 subjects. A significant increase in force generation was seen in eccentric activity at 0.52 rads x s(-1) (30 degrees s(-1)) but not at 1.57 rads x s(-1) (90 degrees s(-1)) compared to maximum voluntary isometric force (P < 0.005). This increase was, however, lower than would be expected from the classical force-velocity relationship. The second part of the study examined whether restricting the range of movement was able to further increase the eccentric forces. In a further 6 subjects, the eccentric contractions were repeated during either an 80 degrees (15-95 degrees flexion) and a 50 degrees (45-95 degrees flexion) range of movement. Significant increases in force were seen over the shorter range of movement at 0.52 rads x s(-1) (30 degrees s(-1)) (P = 0.006) and 1.57 rads x s(-1) (90 degrees s(-1)) (P < 0.001).     

Dynamic chromatin accessibility tuning by the long noncoding RNA ELDR accelerates chondrocyte senescence and osteoarthritis

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A global verification study of a quasi-static knee model with multi-bundle ligaments

The ligaments of the knee consist of fiber bundles with variable orientations, lengths and mechanical properties. In concept, however, these structures were too often seen as homogeneous structures, which are either stretched or slack during knee motions. In previous studies, we proposed a new structural concept of the ligaments of the knee. In this concept, the ligaments were considered as multi-bundle structures, with nonuniform mechanical properties and zero force lengths. The purpose of the present study was to verify this new concept.

For this purpose, laxity characteristics of a human knee joint were compared as measured in an experiment and predicted in a model simulation study. In the experiment, the varus-valgus and anterior-posterior laxities of a knee-joint specimen containing the ligaments and the articular surfaces only, were determined. From this knee-joint, geometric and mechanical parameters were derived to supply the parameters for a three-dimensional quasi-static knee-joint model. These parameters included (i) the three-dimensional insertion points of bundles, defined in the four major knee ligaments, (ii) the mechanical properties of these ligament, as functions of their relative insertion orientations and (iii) three-dimensional representations of the articular surfaces. With this model the experiments were simulated. If knee-model predictions and experimental results agree, then the multi-bundle ligament models are validated, at least with respect to their functional role in anterior-posterior and varus-valgus loading of the joint.

The model described the laxity characteristics in AP-translation and VV-rotation of the cadaveric knee-joint specimen reasonably well. Both display the same patterns of laxity changes during knee flexion. Only if a varus moment of 8 N m was applied and if the tibia was posteriorly loaded, did the model predict a slightly higher laxity than that measured experimentally.

From the model-experiment comparisons it was concluded that the proposed structural representations of the ligaments and their mechanical property distributions seem to be valid for studying the anterior-posterior and varus-valgus laxity characteristics of the human knee-joint.     

Life conditions of a roman imperial age population: Occupational stress markers and working activities inLucus Feroniae (Rome, 1st–2nd cent. AD)

In ancient populations studies, investigation on activity-induced pathology performed by means of an integrated and epidemiological approach can provide useful evidence about physical activities, age of occupancy, sexual differentiation, social stratification and working tasks division of past human groups. The analysis of occupational stress of the skeletal sample coming from the poor necropolis of Lucus Feroniae, a rural town of the Roman Imperial Age, was carried out on: degenerative disease of joints and vertebral bodies, traumas, hypertrophic changes at sites of muscles and ligament insertion, presence of anatomical variants caused by postural habits or body movements. The results as a whole seem to indicate that the population, likely representative of a low social group (potentially slaves), was precociously and actively employed in heavy manual work activities. These may have included farming tasks demanding lifting, heavy loads transportation and long-distance walking on rough grounds.     

Type III collagen is a key regulator of the collagen fibrillar structure and biomechanics of articular cartilage and meniscus

Despite the fact that type III collagen is the second most abundant collagen type in the body, its contribution to the physiologic maintenance and repair of skeletal tissues remains poorly understood. This study queried the role of type III collagen in the structure and biomechanical functions of two structurally distinctive tissues in the knee joint, type II collagen-rich articular cartilage and type I collagen-dominated meniscus. Integrating outcomes from atomic force microscopy-based nanomechanical tests, collagen fibril nanostructural analysis, collagen cross-link analysis and histology, we elucidated the impact of type III collagen haplodeficiency on the morphology, nanostructure and biomechanical properties of articular cartilage and meniscus in Col3a1^+/− mice. Reduction of type III collagen leads to increased heterogeneity and mean thickness of collagen fibril diameter, as well as reduced modulus in both tissues, and these effects became more pronounced with skeletal maturation. These data suggest a crucial role of type III collagen in mediating fibril assembly and biomechanical functions of both articular cartilage and meniscus during post-natal growth. In articular cartilage, type III collagen has a marked contribution to the micromechanics of the pericellular matrix, indicating a potential role in mediating the early stage of type II collagen fibrillogenesis and chondrocyte mechanotransduction. In both tissues, reduction of type III collagen leads to decrease in tissue modulus despite the increase in collagen cross-linking. This suggests that the disruption of matrix structure due to type III collagen deficiency outweighs the stiffening of collagen fibrils by increased cross-linking, leading to a net negative impact on tissue modulus. Collectively, this study is the first to highlight the crucial structural role of type III collagen in both articular cartilage and meniscus extracellular matrices. We expect these results to expand our understanding of type III collagen across various tissue types, and to uncover critical molecular components of the microniche for regenerative strategies targeting articular cartilage and meniscus repair.     

Lysophosphatidic acid mediates migration of human mesenchymal stem cells stimulated by synovial fluid of patients with rheumatoid arthritis

Migration of mesenchymal stem cells plays a key role in regeneration of injured tissues. Rheumatoid arthritis (RA) is a chronic inflammatory disease and synovial fluid (SF) reportedly contains a variety of chemotactic factors. This study was undertaken to investigate the role of SF in migration of human bone marrow-derived mesenchymal stem cells (hBMSCs) and the molecular mechanism of SF-induced cell migration. SF from RA patients greatly stimulated migration of hBMSCs and the SF-induced migration was completely abrogated by pretreatment of the cells with the lysophosphatidic acid (LPA) receptor antagonist Ki16425 and by small interfering RNA- or lentiviral small hairpin RNA-mediated silencing of endogenous LPA₁/Edg2. Moreover, SF from RA patients contains higher concentrations of LPA and an LPA-producing enzyme autotoxin than normal SF. In addition, SF from RA patients increased the intracellular concentration of calcium through a Ki16425-sensitive mechanism and pretreatment of the cells with the calmodulin inhibitor W7 or calmodulin-dependent protein kinase II inhibitor KN93 abrogated the SF-induced cell migration. These results suggest that LPA-LPA₁ plays a key role in the migration of hBMSCs induced by SF from RA patients through LPA₁-dependent activation of calmodulin-dependent protein kinase II.