A Mechanism to Explain Physiological Lubrication

2010 ◽  
Vol 132 (7) ◽  
Author(s):  
David F. James ◽  
Garret M. Fick ◽  
W. Douglas Baines

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.

Cells ◽  
2020 ◽  
Vol 9 (7) ◽  
pp. 1606 ◽  
Author(s):  
Weifeng Lin ◽  
Zhang Liu ◽  
Nir Kampf ◽  
Jacob Klein

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.


Soft Matter ◽  
2014 ◽  
Vol 10 (32) ◽  
pp. 5965-5973 ◽  
Author(s):  
Z. Zhang ◽  
S. Barman ◽  
G. F. Christopher

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


Author(s):  
H Higaki ◽  
T Murakami ◽  
Y Nakanishi ◽  
H Miura ◽  
T Mawatari ◽  
...  

Two kinds of friction tests were conducted to investigate the lubricating effect of the injection of amphiphilies on the osteoarthritic joint. The effects of the addition of Lα-dipalmitoyl phosphatidylcholine (Lα-DPPC) riposomes and γ-globulin in a saline solution of sodium hyaluronate (HA) were evaluated through pendulum friction tests. The frictional characteristics of pig shoulder joints were confirmed to depend on the viscosity of the lubricants only in the physiologically low load condition and in the condition immediately after loading. Detergent (polyoxyethylene p-t-octylphenyl ether) was successfully used to remove adsorbed films from the articular surfaces. The friction coefficient of natural synovial joints was significantly increased in a mode of mixed lubrication with the HA solution of 0.2 g/dl by the treatment of the surface with the detergent. The addition of Lα-DPPC riposomes or y-globulin significantly improved the boundary lubricating ability of the articular surfaces treated with the detergent, depending on the quantity of those additives. It appears that the Lα-DPPC riposomes and γ-globulin can form protective films on the articular surfaces like a biomembrane. Moreover, the reciprocating frictional behaviour in sliding pairs of pig articular cartilages and glass plates was studied in order to elucidate the tribological role of those constituents in the boundary lubricating film on the articular surface. Pig synovial fluid and water solutions of HA were used as lubricants. The synovial fluid had superior lubricating ability compared to the HA solution of equivalent viscosity under a physiologically high load condition. This fact seems to be responsible for the boundary lubricating ability of constituents other than hyaluronic acid. Langmuir-Blodgett (LB) films of Lα-DPPC on the glass plate were kept at a low and stable friction coefficient, depending on the number of film layers. In conditions of mixed films with Lα-DPPC and γ-globulin, the frictional behaviour was improved by increasing the quantity of γ-globulin. A model is proposed in which the effective adsorbed films are composed of proteins, phospholipids and other conjugated constituents on the articular surfaces to be accurate in describing the boundary lubricating mechanism. The mechanism is controlled by hydrophobic groups in those amphiphilies.


Tribologia ◽  
2017 ◽  
Vol 273 (3) ◽  
pp. 127-136
Author(s):  
Andrzej RYNIEWICZ ◽  
Anna RYNIEWICZ

The purpose of the paper is to explain the friction conditions and the lubrication mechanism in healthy joints, based on rheological tests of synovial fluid and the identification of structures and the shape of articular surfaces. The tests were performed on cadaver preparations of large lower limp joints: hip, knee, and ankle joints. The analysis included combined experimental activities with the use of modern research and test techniques in the area of viscosity and microscopy as well as diagnostic imaging, image analysis, modelling, and FEM simulation. The tests performed allowed for the analysis of lubrication process which can be described as bioelastohydrodynamic lubrication (BEHL). The most important are viscoelasticity properties of the synovial fluid and the process whereby the external load is taken over by the pressure generated by a set of oil wedges of synovial fluid formed by naturally wavy articular surface. The multi-layer structure of the joints is characterised by variable wavy shape of cartilaginous surfaces and of bone tissue and by the variable wavy thickness of the cartilage.


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

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Wei Zhang ◽  
Guoyu Yin ◽  
Heping Zhao ◽  
Hanzhi Ling ◽  
Zhen Xie ◽  
...  

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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