Abstract
Articular cartilage injury and repair is an issue of growing importance. Although common, defects of articular cartilage present a unique clinical challenge due to its poor self-healing capacity, which is largely due to its avascular nature. There is a critical need to better study and understand cellular healing mechanisms to achieve more effective therapies for cartilage regeneration. This article aims to describe the key features of cartilage which is being modelled using tissue engineered cartilage constructs and ex vivo systems. These models have been used to investigate chondrogenic differentiation and to study the mechanisms of cartilage integration into the surrounding tissue. The review highlights the key regeneration principles of articular cartilage repair in healthy and diseased joints. Using co-culture models and novel bioreactor designs, the basis of regeneration is aligned with recent efforts for optimal therapeutic interventions.
Highlights
Differentiation and CartilageArticular cartilage, which covers the osseous ends in diarthrodial joints, is an anisotropic tissue with a complex structure
[295]in(Figure result of the absence of shear the uniaxial compression studies, and in agreement with the other studies, compression alone did not lead to chondrogenic induction [295]
The most advanced ex vivo models include the co-culture of at least two different cell the other studies, compression alone did not lead to chondrogenic induction [295]
Summary
Articular cartilage, which covers the osseous ends in diarthrodial joints, is an anisotropic tissue with a complex structure. These factors attract vessels and mesenchymal progenitors into the defect [17] This repair response often leads to the generation of a mechanically inferior fibrocartilage-like repair tissue, which is unable to withstand normal joint load and degenerates further [18]. Release bioactive factors such as platelet derived growth factor (PDGF) and transform- 3 of 32 ing growth factor beta (TGF-β) This repair response often leads to the generation of a mechanically inferior fibrocartilage-like repair tissue, which is unable to withstand normal joint can loadprogress and degenerateswhich furtherultimately [18].
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