From regeneration to osteoarthritis in the knee joint: The role shift of cartilage-derived progenitor cells

Abstract

A mount of growing evidence has proven that cartilage-derived progenitor cells (CPCs) harbor strong proliferation, migration, andmultiple differentiation potentials over the past 2 decades. CPCs in the stage of immature tissue play an important role in cartilage development process and injured cartilage repair in the young and active people. However, during maturation and aging, cartilage defects cannot be completely repaired by CPCs in vivo. Recently, tissue engineering has revealed that repaired cartilage defects with sufficient stem cell resources under good condition and bioactive scaffolds in vitro and in vivo. Chronic inflammation in the knee joint limit the proliferation and chondrogenesis abilities of CPCs, which further hampered cartilage healing and regeneration. Neocartilage formation was observed in the varus deformity of osteoarthritis (OA) patients treated with offloading technologies, which raises the possibility that organisms could rebuild cartilage structures spontaneously. In addition, nutritionmetabolismdysregulation, including glucose and free fatty acid dysregulation, could influence both chondrogenesis and cartilage formation. There are a few reviews about the advantages of CPCs for cartilage repair, but few focused on the reasons why CPCs could not repair the cartilage as they do in immature status. A wide spectrum of CPCs was generated by different techniques and exhibited substantial differences. We recently reported that CPCs maybe are as internal inflammation sources during cartilage inflammaging. In this review, we further streamlined the changes of CPCs from immature development to maturation and from healthy status to OA advancement. The key words including “cartilage derived stem cells”, “cartilage progenitor cells”, “chondroprogenitor cells”, “chondroprogenitors” were set for latest literature searching in PubMed and Web of Science. The articles were then screened through titles, abstracts, and the full texts in sequence. The internal environment including long-term inflammation, extendedmechanical loading, and nutritional elements intake and external deleterious factors were summarized. Taken together, these results provide a comprehensive understanding of the underlying mechanism of CPC proliferation and differentiation during development, maturation, aging, injury, and cartilage regeneration in vivo.

TMF suppresses chondrocyte hypertrophy in osteoarthritic cartilage by mediating the FOXO3a/BMPER pathway

“…It is essential to explore the dose response and time-dependence of TMF on chondrocyte hypertrophy in OA cartilage, and these were not determined in the present study. In vitro study, two concentrations of TMF were studied to inhibit the expression of ColX and Runx-2, which are the biomarkers of OA chondrocyte hypertrophy (64). However, the absence of more concentrations to validate the concentration-dependent TMF inhibition of OA chondrocyte hypertrophy was also a limitation of the present study.…”

Cartilage tissue from sites of weight bearing in patients with osteoarthritis exhibits a differential phenotype with distinct chondrocytes subests

“…As previous studies have revealed, initially, CPCs situated in the superficial layer become activated and proliferate to fill the area with FCs. 74 75 However, only a small fraction of FCs have the ability to differentiate into SCs and migrate towards the deeper layers of cartilage tissue. 76 As the SCs mature, they undergo a transformation into HCs that are typically found at the tidemark of the cartilage tissue.…”

Prg4-Expressing Chondroprogenitor Cells in the Superficial Zone of Articular Cartilage

“…The regenerative potential of chondroprogenitor cells in adult AC tissues is a topic of debate. Prg4-producing cells inhabit both the SFZ of cartilage and the synovial membrane [ 20 , 75 , 76 ]. Using the osteochondral defect model, Decker and collaborators [ 68 ] showed that the injury site was filled by the progeny of Prg4-positive cells within 7 days after surgery.…”