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 ◽  
...  

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.

Author(s):  
M H Naka ◽  
Y Morita ◽  
K Ikeuchi

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.


2017 ◽  
Vol 58 (5) ◽  
pp. 863-873 ◽  
Author(s):  
Lai Ma ◽  
Dechun Zhang ◽  
Qisong Miao ◽  
Jing Yang ◽  
Yuanhu Xuan ◽  
...  

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.


Author(s):  
Jonathan T. Henderson ◽  
Corey P. Neu

Osteoarthritis (OA) is a disabling disease, commonly thought of as the “wear and tear” of articular cartilage, afflicting 27 million Americans [1]. Multiple (e.g. biomechanical and biochemical) factors [2] contribute to maintenance of healthy joints through chondrocyte and extracellular matrix interactions. Interestingly, volumetric contractions of nuclei exhibit a zonal dependence [3], suggesting that nuclear mechanics may play a key role in the maintenance of healthy tissue by mechanically-mediated pathways.


2019 ◽  
Vol 7 (7) ◽  
pp. 1027-1044 ◽  
Author(s):  
D. Bicho ◽  
S. Ajami ◽  
C. Liu ◽  
R. L. Reis ◽  
J. M. Oliveira

Osteoarthritis is a degenerative joint disease characterized by the progressive deterioration of articular cartilage, synovial inflammation and changes in periarticular and subchondral bone, being a leading cause of disability.


2014 ◽  
Vol 2014 ◽  
pp. 1-19 ◽  
Author(s):  
Piotr Wojdasiewicz ◽  
Łukasz A. Poniatowski ◽  
Dariusz Szukiewicz

Osteoarthritis (OA) is the most common chronic disease of human joints. The basis of pathologic changes involves all the tissues forming the joint; already, at an early stage, it has the nature of inflammation with varying degrees of severity. An analysis of the complex relationships indicates that the processes taking place inside the joint are not merely a set that (seemingly) only includes catabolic effects. Apart from them, anti-inflammatory anabolic processes also occur continually. These phenomena are driven by various mediators, of which the key role is attributed to the interactions within the cytokine network. The most important group controlling the disease seems to be inflammatory cytokines, including IL-1β, TNFα, IL-6, IL-15, IL-17, and IL-18. The second group with antagonistic effect is formed by cytokines known as anti-inflammatory cytokines such as IL-4, IL-10, and IL-13. The role of inflammatory and anti-inflammatory cytokines in the pathogenesis of OA with respect to inter- and intracellular signaling pathways is still under investigation. This paper summarizes the current state of knowledge. The cytokine network in OA is put in the context of cells involved in this degenerative joint disease. The possibilities for further implementation of new therapeutic strategies in OA are also pointed.


2016 ◽  
Vol 113 (50) ◽  
pp. 14360-14365 ◽  
Author(s):  
Haoruo Jia ◽  
Xiaoyuan Ma ◽  
Wei Tong ◽  
Basak Doyran ◽  
Zeyang Sun ◽  
...  

Osteoarthritis (OA) is the most common joint disease, characterized by progressive destruction of the articular cartilage. The surface of joint cartilage is the first defensive and affected site of OA, but our knowledge of genesis and homeostasis of this superficial zone is scarce. EGFR signaling is important for tissue homeostasis. Immunostaining revealed that its activity is mostly dominant in the superficial layer of healthy cartilage but greatly diminished when OA initiates. To evaluate the role of EGFR signaling in the articular cartilage, we studied a cartilage-specific Egfr-deficient (CKO) mouse model (Col2-Cre EgfrWa5/flox). These mice developed early cartilage degeneration at 6 mo of age. By 2 mo of age, although their gross cartilage morphology appears normal, CKO mice had a drastically reduced number of superficial chondrocytes and decreased lubricant secretion at the surface. Using superficial chondrocyte and cartilage explant cultures, we demonstrated that EGFR signaling is critical for maintaining the number and properties of superficial chondrocytes, promoting chondrogenic proteoglycan 4 (Prg4) expression, and stimulating the lubrication function of the cartilage surface. In addition, EGFR deficiency greatly disorganized collagen fibrils in articular cartilage and strikingly reduced cartilage surface modulus. After surgical induction of OA at 3 mo of age, CKO mice quickly developed the most severe OA phenotype, including a complete loss of cartilage, extremely high surface modulus, subchondral bone plate thickening, and elevated joint pain. Taken together, our studies establish EGFR signaling as an important regulator of the superficial layer during articular cartilage development and OA initiation.


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