scholarly journals The Role of Hyaluronic Acid in Cartilage Boundary Lubrication

Cells ◽  
2020 ◽  
Vol 9 (7) ◽  
pp. 1606 ◽  
Author(s):  
Weifeng Lin ◽  
Zhang Liu ◽  
Nir Kampf ◽  
Jacob Klein
Keyword(s):  
Hyaluronic Acid ◽  
Synovial Fluid ◽  
Surface Force ◽  
Force Balance ◽  
New Paradigm ◽  
Low Friction ◽  
Cartilage Surface ◽  
Boundary Lubricant ◽  
Lipid Layers

Hydration lubrication has emerged as a new paradigm for lubrication in aqueous and biological media, accounting especially for the extremely low friction (friction coefficients down to 0.001) of articular cartilage lubrication in joints. Among the ensemble of molecules acting in the joint, phosphatidylcholine (PC) lipids have been proposed as the key molecules forming, in a complex with other molecules including hyaluronic acid (HA), a robust layer on the outer surface of the cartilage. HA, ubiquitous in synovial joints, is not in itself a good boundary lubricant, but binds the PC lipids at the cartilage surface; these, in turn, massively reduce the friction via hydration lubrication at their exposed, highly hydrated phosphocholine headgroups. An important unresolved issue in this scenario is why the free HA molecules in the synovial fluid do not suppress the lubricity by adsorbing simultaneously to the opposing lipid layers, i.e., forming an adhesive, dissipative bridge between them, as they slide past each other during joint articulation. To address this question, we directly examined the friction between two hydrogenated soy PC (HSPC) lipid layers (in the form of liposomes) immersed in HA solution or two palmitoyl–oleoyl PC (POPC) lipid layers across HA–POPC solution using a surface force balance (SFB). The results show, clearly and surprisingly, that HA addition does not affect the outstanding lubrication provided by the PC lipid layers. A possible mechanism indicated by our data that may account for this is that multiple lipid layers form on each cartilage surface, so that the slip plane may move from the midplane between the opposing surfaces, which is bridged by the HA, to an HA-free interface within a multilayer, where hydration lubrication is freely active. Another possibility suggested by our model experiments is that lipids in synovial fluid may complex with HA, thereby inhibiting the HA molecules from adhering to the lipids on the cartilage surfaces.

The role of protein content on the steady and oscillatory shear rheology of model synovial fluids

Soft Matter ◽  
2014 ◽  
Vol 10 (32) ◽  
pp. 5965-5973 ◽  
Author(s):  
Z. Zhang ◽  
S. Barman ◽  
G. F. Christopher
Keyword(s):  
Hyaluronic Acid ◽  
Synovial Fluid ◽  
Acid Solution ◽  
Protein Content ◽  
Shear Viscosity ◽  
Steady Shear ◽  
Interfacial Rheology ◽  
Steady Shear Viscosity ◽  
Synovial Fluids

Model synovial fluid steady shear viscosity to hyaluronic acid solution are identical when interfacial rheology effects are removed.

scholarly journals Recent Advances in Understanding the Role of Cartilage Lubrication in Osteoarthritis

Molecules ◽  
2021 ◽  
Vol 26 (20) ◽  
pp. 6122
Author(s):  
Yumei Li ◽  
Zhongrun Yuan ◽  
Hui Yang ◽  
Haijian Zhong ◽  
Weijie Peng ◽  
...  
Keyword(s):  
Articular Cartilage ◽  
Essential Role ◽  
Daily Life ◽  
Early Stage ◽  
Joint Disease ◽  
Low Friction ◽  
Cartilage Surface ◽  
Wear And Tear ◽  
Lubrication Properties

The remarkable lubrication properties of normal articular cartilage play an essential role in daily life, providing almost frictionless movements of joints. Alterations of cartilage surface or degradation of biomacromolecules within synovial fluid increase the wear and tear of the cartilage and hence determining the onset of the most common joint disease, osteoarthritis (OA). The irreversible and progressive degradation of articular cartilage is the hallmark of OA. Considering the absence of effective options to treat OA, the mechanosensitivity of chondrocytes has captured attention. As the only embedded cells in cartilage, the metabolism of chondrocytes is essential in maintaining homeostasis of cartilage, which triggers motivations to understand what is behind the low friction of cartilage and develop biolubrication-based strategies to postpone or even possibly heal OA. This review firstly focuses on the mechanism of cartilage lubrication, particularly on boundary lubrication. Then the mechanotransduction (especially shear stress) of chondrocytes is discussed. The following summarizes the recent development of cartilage-inspired biolubricants to highlight the correlation between cartilage lubrication and OA. One might expect that the restoration of cartilage lubrication at the early stage of OA could potentially promote the regeneration of cartilage and reverse its pathology to cure OA.

A Mechanism to Explain Physiological Lubrication

2010 ◽  
Vol 132 (7) ◽  
Author(s):  
David F. James ◽  
Garret M. Fick ◽  
W. Douglas Baines
Keyword(s):  
Hyaluronic Acid ◽  
Synovial Fluid ◽  
Articular Surface ◽  
Constant Load ◽  
Squeeze Film ◽  
Hydrodynamic Resistance ◽  
Low Viscosity ◽  
Electrostatic Charges ◽  
Articular Surfaces

A new mechanism of physiological lubrication is proposed to explain how low-viscosity synovial fluid prevents articular surfaces from contacting and wearing. The new mechanism is based on the hypothesis that the hyaluronic acid chains in synovial fluid bind to the cartilage surfaces through electrostatic charges, with the phospholipid layer on an articular surface supplying the necessary attractive charges. The stationary hyaluronic acid network causes a large hydrodynamic resistance to outward flow from the gap. To determine the effectiveness of the network in preventing contact, squeeze-film flow between two incompressible, permeable disks is analyzed when a constant load is suddenly applied, and the solvent—synovial fluid minus the hyaluronic acid—escapes through the network and through the permeable disks. The analysis yields the approximate time for the gap distance to decrease to asperity size. For realistic physiological parameters, the time for the surfaces to contact is a minimum of several minutes and likely much longer. The role of albumin in the synovial fluid is included because the large protein molecules are trapped by the small openings in the hyaluronic acid network, which increases the flow resistance of the network and thereby delays contact of the surfaces.

Lubricin Interaction With Hyaluronate Promotes Interchain Association Leading to Network Formation

2005 ◽  
Author(s):  
J. R. Torres ◽  
G. D. Jay ◽  
M. L. Warman ◽  
R. M. Laxer ◽  
M. Laderer ◽  
...  
Keyword(s):  
Mechanical Properties ◽  
Synovial Fluid ◽  
Particle Tracking ◽  
Network Formation ◽  
Molecular Layering ◽  
Cartilage Surface ◽  
Particle Tracking Microrheology ◽  
Boundary Lubricant ◽  
Multiple Particle Tracking ◽  
Multiple Particle

The present work is the first instance where a novel multiple-particle tracking microrheology technique has been applied to study molecular interactions of clinical significance. Herein we describe the molecular changes due to lubricin-hyaluronate interaction and their effect on mechanical properties of synovial fluid. Along with bulk rheology studies it was found that lubricin, a boundary lubricant, increases the HA network formation conducive to the enhanced molecular layering of HA under stress which results in increased shear thinning. This interaction may also allow HA molecules to bind to the cartilage surface, providing boundary lubrication, by virtue of its interaction with lubricin.

Influence of proteoglycan contents and of tissue hydration on the frictional characteristics of articular cartilage

2005 ◽  
Vol 219 (3) ◽  
pp. 175-182 ◽  
Author(s):  
M H Naka ◽  
Y Morita ◽  
K Ikeuchi
Keyword(s):  
Articular Cartilage ◽  
Water Content ◽  
Articular Surface ◽  
Superficial Layer ◽  
Low Friction ◽  
Cartilage Surface ◽  
Intact Condition ◽  
Measured Water ◽  
Femoral Condyles

In this work, the hypothesis that water content and substances present on the articular surface play an important role in lubrication through the formation of a layer with a high content of water on the articular surface is analysed. The hydrophilic properties of proteoglycans exposed at the articular surface and hydration of tissue are the main responsible factors for the formation of this layer. The role of the articular surface in the frictional characteristics of articular cartilage was examined using specimens (femoral condyles of pigs) with intact and wiped surfaces tested in intermittent friction tests. Results indicated that the intact condition presented low friction in comparison with the wiped condition. The measured water loss of the articular cartilage after sliding and loading indicated a gradual decrease in the water content as the time evolved, and rehydration was observed after the submersion of unloaded specimens in the saline bath solution. Micrographic analyses indicated the presence of a layer covering the articular surface, and histological analyses indicated the presence of proteoglycans in this superficial layer. The hydration of the cartilage surface layer and proteoglycan in this layer influence lubrication.

Polymer displacement and the role of impurities in homopolymer adsorption: a surface force balance study

Langmuir ◽  
1991 ◽  
Vol 7 (10) ◽  
pp. 2346-2352 ◽  
Author(s):  
David A. Guzonas ◽  
Michael L. Hair
Keyword(s):  
Surface Force ◽  
Force Balance ◽  
Balance Study

INOVASI PEMBELAJARAN AKIDAH AKHLAK MENGGUNAKAN METODE ROLE PLAY DALAM MENINGKATKAN PRESTASI BELAJAR SISWA

2018 ◽  
Vol 2 (1) ◽  
pp. 52-63
Author(s):  
Ansori Ansori
Keyword(s):  
Data Reduction ◽  
Role Play ◽  
Learning Goals ◽  
New Paradigm ◽  
Learning Materials ◽  
Analysis Technique ◽  
Flexible Schedule ◽  
Using Data ◽  
Real Action

The use of various methods will greatly help students in achieving learning goals. As role play method is one way mastery of learning materials through the development of imagination and appreciation of students on learning materials. Data collection techniques in this study are observation, interviews, and documentation. To analyze the data in this research using data analysis technique of Miles and Huberman model that is data reduction (Data Reduction), data presentation (Data Display) and conclusion (Conclution Drawing / verification) The findings in this research is innovation of role play method can change paradigm to the new paradigm so that the role of the teacher is more as a facilitator, counselor, consultant, and comrade study Flexible schedule, open as needed Learning directed by students themselves Problem-based, project, real world, real action, and reflection Design and investigation. Computers as tools, and dynamic media presentations.

scholarly journals Hyaluronic Acid in Synovial Fluid

1970 ◽  
Vol 11 (2) ◽  
pp. 139-155 ◽  
Author(s):  
Nils W. Rydell ◽  
Judson Butler ◽  
Endre A. Balazs
Keyword(s):  
Hyaluronic Acid ◽  
Synovial Fluid

scholarly journals Secreted KIAA1199 promotes the progression of rheumatoid arthritis by mediating hyaluronic acid degradation in an ANXA1-dependent manner

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Wei Zhang ◽  
Guoyu Yin ◽  
Heping Zhao ◽  
Hanzhi Ling ◽  
Zhen Xie ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Hyaluronic Acid ◽  
Dependent Manner ◽  
Collagen Induced Arthritis ◽  
Intracellular Degradation ◽  
Main Pathway ◽  
First Time

AbstractIn inflamed joints, enhanced hyaluronic acid (HA) degradation is closely related to the pathogenesis of rheumatoid arthritis (RA). KIAA1199 has been identified as a hyaladherin that mediates the intracellular degradation of HA, but its extracellular function remains unclear. In this study, we found that the serum and synovial levels of secreted KIAA1199 (sKIAA1199) and low-molecular-weight HA (LMW-HA, MW < 100 kDa) in RA patients were significantly increased, and the positive correlation between them was shown for the first time. Of note, treatment with anti-KIAA1199 mAb effectively alleviated the severity of arthritis and reduced serum LMW-HA levels and cytokine secretion in collagen-induced arthritis (CIA) mice. In vitro, sKIAA1199 was shown to mediate exogenous HA degradation by attaching to the cell membrane of RA fibroblast-like synoviosytes (RA FLS). Furthermore, the HA-degrading activity of sKIAA1199 depended largely on its adhesion to the membrane, which was achieved by its G8 domain binding to ANXA1. In vivo, kiaa1199-KO mice exhibited greater resistance to collagen-induced arthritis. Interestingly, this resistance could be partially reversed by intra-articular injection of vectors encoding full-length KIAA1199 instead of G8-deleted KIAA119 mutant, which further confirmed the indispensable role of G8 domain in KIAA1199 involvement in RA pathological processes. Mechanically, the activation of NF-κB by interleukin-6 (IL-6) through PI3K/Akt signaling is suggested to be the main pathway to induce KIAA1199 expression in RA FLS. In conclusion, our study supported the contribution of sKIAA1199 to RA pathogenesis, providing a new therapeutic target for RA by blocking sKIAA1199-mediated HA degradation.

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