Articular fibrocartilage - Why does hyaline cartilage fail to repair?

被引：287

作者：

Armiento, Angela R. ^{[1
]}

Alini, Mauro ^{[1
]}

Stoddart, Martin J. ^{[1
]}

机构：

[1] AO Res Inst Davos, Clavadelerstr 8, CH-7270 Davos, Switzerland

来源：

ADVANCED DRUG DELIVERY REVIEWS | 2019年 / 146卷

关键词：

Chondrocytes; Cartilage; Mesenchymal stem cells; Differentiation; Chondrogenesis; Paracrine; Secretome; Cytoki nes; Gene therapy; MESENCHYMAL STEM-CELLS; OLIGOMERIC MATRIX PROTEIN; AUTOLOGOUS CHONDROCYTE IMPLANTATION; COLLAGEN TYPE-II; LEUCINE-RICH PROTEOGLYCANS; T-LYMPHOCYTE PROLIFERATION; HYALURONIC-ACID HYDROGELS; TISSUE SHEAR DEFORMATION; IN-VITRO CHONDROGENESIS; GROWTH-FACTOR-I;

D O I：

10.1016/j.addr.2018.12.015

中图分类号：

R9 [药学];

学科分类号：

100702 [药剂学];

摘要：

Once damaged, articular cartilage has a limited potential to repair. Clinically, a repair tissue is formed, yet, it is often mechanically inferior fibrocartilage. The use of monolayer expanded versus naive cells may explain one of the biggest discrepancies in mesenchymal stromal/stem cell (MSC) based cartilage regeneration. Namely, studies utilizing monolayer expanded MSCs, as indicated by numerous in vitro studies, report as a main limitation the induction of type X collagen and hypertrophy, a phenotype associated with endochondral bone formation. However, marrow stimulation and transfer studies report a mechanically inferior collagen I/II fibrocartilage as the main outcome. Therefore, this review will highlight the collagen species produced during the different therapeutic approaches. New developments in scaffold design and delivery of therapeutic molecules will be described. Potential future directions towards clinical translation will be discussed. New delivery mechanisms are being developed and they offer new hope in targeted therapeutic delivery. (C) 2019 The Authors. Published by Elsevier B.V.

引用

页码：289 / 305

页数：17

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