scholarly journals P112 Alterations of calcified cartilage and subchondral bone observed in osteoarthritic joints: A stereological study in two strains of guinea pig

2005 ◽  
Vol 13 ◽  
pp. S61-S62
Author(s):  
Mengtao Liu ◽  
Xiurong Ke ◽  
Yuejun Yao ◽  
Fanghui Wu ◽  
Shuo Ye ◽  
...  

Calcified cartilage is a mineralized osteochondral interface region between the hyaline cartilage and subchondral bone, whereas there were few reported artificial biomaterials that could offer bioactivities for substantial reconstruction of...


2020 ◽  
Vol 2020 ◽  
pp. 1-8
Author(s):  
Xuchang Zhou ◽  
Hong Cao ◽  
Yu Yuan ◽  
Wei Wu

Osteochondral junction is a functional unit comprising the articular cartilage, calcified cartilage, and subchondral bone. Alteration in any component of this composite unit can disrupt the joint integrity and function directly or indirectly. Biochemical signals mediate the crosstalk between tissues and play an essential role in the initiation and progression of osteoarthritis. As osteoarthritis progresses, abnormal subchondral bone remodelling leads to increased angiogenesis and porosity of the subchondral bone plate, which further triggers biochemical signals to mediate the crosstalk between cartilage and bone, contributing to the progression of osteoarthritis. Notably, common biochemical signals include the TGF-β/Smad, Wnt/β-catenin, RANK/RANKL/OPG, and MAPK pathways. This biomarker crosstalk network is the basis of osteoarthritis pathogenesis, and some of their key regulators may be potential therapeutic targets for osteoarthritis drug therapy. This review summarised the biochemical crosstalk between cartilage and bone in the pathogenesis of osteoarthritis, which may provide the basis for the discovery of osteoarthritis treatment targets.


2015 ◽  
Vol 23 (10) ◽  
pp. 1755-1762 ◽  
Author(s):  
E. Hargrave-Thomas ◽  
F. van Sloun ◽  
M. Dickinson ◽  
N. Broom ◽  
A. Thambyah

2019 ◽  
Vol 27 ◽  
pp. S160-S161
Author(s):  
S. Das Gupta ◽  
M.A. Finnilä ◽  
S.S. Karhula ◽  
R. Korhonen ◽  
A. Thambyah ◽  
...  

Bone ◽  
1999 ◽  
Vol 24 (2) ◽  
pp. 109-114 ◽  
Author(s):  
R.W Norrdin ◽  
C.E Kawcak ◽  
B.A Capwell ◽  
C.W McIlwraith

2012 ◽  
Vol 4 (4) ◽  
pp. 249-258 ◽  
Author(s):  
Steven R. Goldring

The articular cartilage and the subchondral bone form a biocomposite that is uniquely adapted to the transfer of loads across the diarthrodial joint. During the evolution of the osteoarthritic process biomechanical and biological processes result in alterations in the composition, structure and functional properties of these tissues. Given the intimate contact between the cartilage and bone, alterations of either tissue will modulate the properties and function of the other joint component. The changes in periarticular bone tend to occur very early in the development of OA. Although chondrocytes also have the capacity to modulate their functional state in response to loading, the capacity of these cells to repair and modify their surrounding extracellular matrix is relatively limited in comparison to the adjacent subchondral bone. This differential adaptive capacity likely underlies the more rapid appearance of detectable skeletal changes in OA in comparison to the articular cartilage. The OA changes in periarticular bone include increases in subchondral cortical bone thickness, gradual decreases in subchondral trabeular bone mass, formation of marginal joint osteophytes, development of bone cysts and advancement of the zone of calcified cartilage between the articular cartilage and subchondral bone. The expansion of the zone of calcified cartilage contributes to overall thinning of the articular cartilage. The mechanisms involved in this process include the release of soluble mediators from chondrocytes in the deep zones of the articular cartilage and/or the influences of microcracks that have initiated focal remodeling in the calcified cartilage and subchondral bone in an attempt to repair the microdamage. There is the need for further studies to define the pathophysiological mechanisms involved in the interaction between subchondral bone and articular cartilage and for applying this information to the development of therapeutic interventions to improve the outcomes in patients with OA.


Author(s):  
Seyed Shayan Sajjadinia ◽  
Mohammad Haghpanahi ◽  
Mohammad Razi

It has been experimentally proposed that the discrete regions of articular cartilage, along with different subchondral bone tissues, known as the bone-cartilage unit, are biomechanically altered during osteoarthritis degeneration. However, a computational framework capturing all of the dominant changes in the multiphasic parameters has not yet been developed. This article proposes a new finite element model of the bone-cartilage unit by combining several validated, nonlinear, depth-dependent, fibril-reinforced, and swelling models, which can computationally simulate the variations in the dominant parameters during osteoarthritis degeneration by indentation and unconfined compression tests. The mentioned dominant parameters include the proteoglycan depletion, collagen fibrillar softening, permeability, and fluid fraction increase for approximately non-advanced osteoarthritis. The results depict the importance of subchondral bone tissues in fluid distribution within the bone-cartilage units by decreasing the fluid permeation and pressure (up to a maximum of 100 kPa) during osteoarthritis, supporting the notion that subchondral bones might play a role in the pathogenesis of osteoarthritis. Furthermore, the osteoarthritis composition-based studies shed light on the significant biomechanical role of the calcified cartilage, which experienced a maximum change of 70 kPa in stress, together with relative load contributions of articular cartilage constituents during osteoarthritis, in which the osmotic pressure bore around 70% of the loads after degeneration. To conclude, the new insights provided by the results reveal the significance of the multiphasic osteoarthritis simulation and demonstrate the functionality of the proposed bone-cartilage unit model.


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