Relaxation capacity of cartilage is a critical factor in rate- and integrity-dependent fracture.
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ABSTRACT:
SUBMITTER: Han G
PROVIDER: S-EPMC8096812 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Possible links between adhesive properties and the pre-sliding (static) friction response of cartilage are not fully understood in the literature. The aims of this study are to investigate the relation between adhesion and relaxation time in articular cartilage, and the effect of relaxation-dependent adhesion on the pre-sliding response of cartilage. Adhesion tests were performed to evaluate the work of adhesion of cartilage at different relaxation times. Friction tests were conducted to identify the pre-sliding friction response of cartilage at relaxation times corresponding to adhesion tests. The pre-sliding friction response of cartilage was systematically linked to the work of adhesion and contact conditions by a slip-based failure model. It was found that the work of adhesion increases with relaxation time. Also, the work of adhesion is linearly correlated to the resistance to slip-based failure. In addition, as the work of adhesion increases, the adhered (stick) area at the moment of failure increases, and the propagation rate of the annular slip (crack) area towards its centre increases. These findings offer a mechanistic explanation of the pre-sliding friction behaviour and stick-slip response of soft hydrated interfaces such as articular cartilage and hydrogels. In addition, the linear correlation between adhesion and threshold to slip-based failure enables estimation of the adhesive strength of such interfaces directly from the pre-sliding friction response (e.g. shear wave elastography).
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Project description:PurposeDaily activities including walking impose high-frequency cyclic forces on cartilage and repetitive compressive deformation. Analyzing cartilage deformation during walking would provide spatial maps of displacement and strain and enable viscoelastic characterization, which may serve as imaging biomarkers for early cartilage degeneration when the damage is still reversible. However, the time-dependent biomechanics of cartilage is not well described, and how defects in the joint impact the viscoelastic response is unclear.MethodsWe used spiral acquisition with displacement-encoding MRI to quantify displacement and strain maps at a high frame rate (25 frames/s) in tibiofemoral joints. We also employed relaxometry methods (T1 , T1ρ , T2 , T2 *) on the cartilage.ResultsNormal and shear strains were concentrated on the bovine tibiofemoral contact area during loading, and the defected joint exhibited larger compressive strains. We also determined a positive correlation between the change of T1ρ in cartilage after cyclic loading and increased compressive strain on the defected joint. Viscoelastic behavior was quantified by the time-dependent displacement, where the damaged joint showed increased creep behavior compared to the intact joint. This technique was also successfully demonstrated on an in vivo human knee showing the gradual change of displacement during varus load.ConclusionOur results indicate that spiral scanning with displacement encoding can quantitatively differentiate the damaged from intact joint using the strain and creep response. The viscoelastic response identified with this methodology could serve as biomarkers to detect defects in joints in vivo and facilitate the early diagnosis of joint diseases such as osteoarthritis.
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Project description:ObjectiveThis work evaluates the rate-dependent and relaxation properties of native porcine heart valves, glutaraldehyde fixed porcine pericardium, and decellularized sterilized porcine pericardium.MethodsBiaxial tension testing was performed at strain-rates of 0.001 s-1, 0.01 s-1, 0.1 s-1, and 1 s-1. Finally, relaxation testing for 300 s was performed on all heart valve biomaterials.ResultsNo notable rate-dependent response was observed for any of the three biomaterials with few significant differences between any strain-rates. For relaxation testing, native tissues showed the most pronounced drop in stress and glutaraldehyde the lowest drop in stress although no tissues showed anisotropy in the relaxation.ConclusionsIncreasing the strain-rate of the three biomaterials considered does not increase the stress within the tissue. This indicates that there will not be increased fatigue from accelerated wear testing compared to loading at physiological strain-rates as the increase strain-rates would likely not significantly alter the tissue stress.
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Project description:Dense suspensions exhibit the remarkable ability to switch dynamically and reversibly from a fluid-like to a solid-like, shear-jammed (SJ) state. Here, we show how this transition has important implications for the propensity for forming fractures. We inject air into bulk dense cornstarch suspensions and visualize the air invasion into the opaque material using time-resolved X-ray radiography. For suspensions with cornstarch mass fractions high enough to exhibit discontinuous shear thickening and shear jamming, we show that air injection leads to fractures in the material. For high mass fractions, these fractures grow quasistatically as rough cavities with fractured interfaces. For lower mass fractions, remarkably, the fractures can relax to smooth bubbles that then rise under buoyancy. We show that the onset of the relaxation occurs as the shear rate induced by the air cavity growth decreases below the critical shear rate denoting the onset of discontinuous shear thickening, which reveals a structural signature of the SJ state.
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Project description:Osteoarthritis (OA) is a widespread chronic joint disease characterized by articular cartilage destruction and accompanied by pain and disability. In this study, we found that the expression of Insulin-like Growth Factor II (IGF-II) was reduced in articular cartilage in human OA patients as well as in the murine experimental OA model of destabilization of the medial meniscus (DMM). In primary human articular chondrocytes, ectopic expression of lentiviral IGF-II inhibited pro-inflammatory cytokine IL-1β-induced NF-κB activation as well as catabolic gene expression. Interestingly, IGF-II did not significantly alter the phosphorylation states of ERK1/2 or Akt, which are kinases typically activated by IGF-I. Instead, it induced the activity of phospholipase C (PLC) and a PLC inhibitor blocked the inhibitory activity of IGF-II against IL-1β, suggesting that this activity is mediated through PLC. Furthermore, IGF-II increased cartilage matrix levels and decreased MMP13 protein expression in explanted human OA cartilage cultures in vitro. In the in vivo DMM model, intraarticular injection of lentiviral IGF-II led to enhanced cartilage matrix levels and decreased MMP13 protein expression, as well as reduced osteophyte formation and subchondral bone sclerosis. Therefore, our results suggest that IGF-II can promote cartilage integrity and halt knee joint destruction in OA.
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Project description:Current therapies for delayed- or nonunion bone fractures are still largely ineffective. Previous studies indicated that the VEGF homolog placental growth factor (PlGF) has a more significant role in disease than in health. Therefore we investigated the role of PlGF in a model of semi-stabilized bone fracture healing. Fracture repair in mice lacking PlGF was impaired and characterized by a massive accumulation of cartilage in the callus, reminiscent of delayed- or nonunion fractures. PlGF was required for the early recruitment of inflammatory cells and the vascularization of the fracture wound. Interestingly, however, PlGF also played a role in the subsequent stages of the repair process. Indeed in vivo and in vitro findings indicated that PlGF induced the proliferation and osteogenic differentiation of mesenchymal progenitors and stimulated cartilage turnover by particular MMPs. Later in the process, PlGF was required for the remodeling of the newly formed bone by stimulating osteoclast differentiation. As PlGF expression was increased throughout the process of bone repair and all the important cell types involved expressed its receptor VEGFR-1, the present data suggest that PlGF is required for mediating and coordinating the key aspects of fracture repair. Therefore PlGF may potentially offer therapeutic advantages for fracture repair.
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Project description:Chemical exchange saturation transfer (CEST) imaging of amides at 3.5 ppm and fast-exchanging amines at 3 ppm provides a unique means to enhance the sensitivity of detection of, for example, proteins/peptides and neurotransmitters, respectively, and hence can provide important information on molecular composition. However, despite the high sensitivity relative to conventional magnetic resonance spectroscopy (MRS), in practice, CEST often has relatively poor specificity. For example, CEST signals are typically influenced by several confounding effects, including direct water saturation (DS), semi-solid non-specific magnetization transfer (MT), the influence of water relaxation times (T1w ) and nearby overlapping CEST signals. Although several editing techniques have been developed to increase the specificity by removing DS, semi-solid MT and T1w influences, it is still challenging to remove overlapping CEST signals from different exchanging sites. For instance, the amide proton transfer (APT) signal could be contaminated by CEST effects from fast-exchanging amines at 3 ppm and intermediate-exchanging amines at 2 ppm. The current work applies an exchange-dependent relaxation rate (Rex ) to address this problem. Simulations demonstrate that: (1) slowly exchanging amides and fast-exchanging amines have distinct dependences on irradiation powers; and (2) Rex serves as a resonance frequency high-pass filter to selectively reduce CEST signals with resonance frequencies closer to water. These characteristics of Rex provide a means to isolate the APT signal from amines. In addition, previous studies have shown that CEST signals from fast-exchanging amines have no distinct features around their resonance frequencies. However, Rex gives Lorentzian lineshapes centered at their resonance frequencies for fast-exchanging amines and thus can significantly increase the specificity of CEST imaging for amides and fast-exchanging amines.
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Project description:Skeletal tissues develop either by intramembranous ossification, where bone is formed within a soft connective tissue, or by endochondral ossification. The latter proceeds via cartilage anlagen, which through hypertrophy, mineralization, and partial resorption ultimately provides scaffolding for bone formation. Here, we describe a novel and essential mechanism governing remodeling of unmineralized cartilage anlagen into membranous bone, as well as tendons and ligaments. Membrane-type 1 matrix metalloproteinase (MT1-MMP)-dependent dissolution of unmineralized cartilages, coupled with apoptosis of nonhypertrophic chondrocytes, mediates remodeling of these cartilages into other tissues. The MT1-MMP deficiency disrupts this process and uncouples apoptotic demise of chondrocytes and cartilage degradation, resulting in the persistence of "ghost" cartilages with adverse effects on skeletal integrity. Some cells entrapped in these ghost cartilages escape apoptosis, maintain DNA synthesis, and assume phenotypes normally found in the tissues replacing unmineralized cartilages. The coordinated apoptosis and matrix metalloproteinase-directed cartilage dissolution is akin to metamorphosis and may thus represent its evolutionary legacy in mammals.
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Project description:Diabetes interferes with fracture repair; therefore, we investigated mechanisms of impaired fracture healing in a model of multiple low-dose streptozotocin-induced diabetes. Microarray and gene set enrichment analysis revealed an up-regulation of gene sets related to inflammation, including tumor necrosis factor (TNF) signaling in the diabetic group, when cartilage is being replaced by bone on day 16, but not on days 12 or 22. This change coincided with elevated osteoclast numbers and accelerated removal of cartilage in the diabetic group (P < 0.05), which was reflected by smaller callus size. When diabetic mice were treated with the TNF-specific inhibitor, pegsunercept, the number of osteoclasts, cartilage loss, and number of TNF-alpha and receptor activator for nuclear factor kB ligand positive chondrocytes were significantly reduced (P < 0.05). The transcription factor forkhead box 01 (FOXO1) was tested for mediating TNF stimulation of osteoclastogenic and inflammatory factors in bone morphogenetic protein 2 pretreated ATDC5 and C3H10T1/2 chondrogenic cells. FOXO1 knockdown by small-interfering RNA significantly reduced TNF-alpha, receptor activator for nuclear factor kB ligand, macrophage colony-stimulating factor, interleukin-1alpha, and interleukin-6 mRNA compared with scrambled small-interfering RNA. An association between FOXO1 and the TNF-alpha promoter was demonstrated by chromatin immunoprecipitation assay. Moreover, diabetes increased FOXO1 nuclear translocation in chondrocytes in vivo and increased FOXO1 DNA binding activity in diabetic fracture calluses (P < 0.05). These results suggest that diabetes-enhanced TNF-alpha increases the expression of resorptive factors in chondrocytes through a process that involves activation of FOXO1 and that TNF-alpha dysregulation leads to enhanced osteoclast formation and accelerated loss of cartilage.
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Project description:Articular cartilage lines synovial joints and functions as a low-friction deformable tissue to enable smooth and stable joint articulation. The objective of this study was to determine the relationships between cartilage stress-relaxation properties and the collagen and GAG NMR transverse relaxation times (T(2)) toward understanding mechanisms of cartilage viscoelasticity. Stress-relaxation tests were performed on both cultured and enzymatically digested bovine cartilage, followed by measurements of both the collagen and GAG T(2) using the Call-Purcell-Meiboom-Gill pulse sequence. The peak and equilibrium stresses were correlated with the GAG T(2), and the stress-relaxation time constant was correlated with the collagen T(2). Multiple linear regression models were successful in using the specific T(2) values to predict the stress-relaxation properties. As a model of osteoarthritis, enzymatic digestion with collagenase and testicular hyaluronidase had weak effects on T(2) values. These data present a complex picture of cartilage mechanical behavior, with cartilage stiffness associated with the GAG T(2) values and the stress-relaxation time constant associated with the collagen T(2).
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