TABLE 1.

The comparison of CPCs from different sources, chondrocytes and BMSCs.

Species	Age	Gender	Sites	Severity	Isolated method	Major results	Ref
Human	Average age: 60.1 years	6 M/9 F	Femoral condyle cartilage	Unaffected areas of OA cartilage	NGF stimulated migration	CPCs were activated by IL1b and NGF signaling in OA.	Jiang and Tuan (2015)
	N = 3			Normal cartilage
	N = 3			Fetal cartilage
Mouse	6 weeks old	Male	Knee articular cartilage	Normal cartilage	Fibronectin attachment	Fibronectin enhanced the proliferation, migration and chondrogenic differentiation capacity of CPCs via the integrin α5β1 pathway	Tao et al. (2018)
Rat	8 weeks old		Articular cartilage	Normal cartilage	Colonies formation	Leptin decreased CPCs migration and chondrogenic potential, meanwhile increased osteogenic potential	Zhao et al. (2016)
Horse	2–8 years old (N = 5)		Distal end of metacarpal bone III	Normal cartilage	Fibronectin attachment	Pellets derived from BMSC expressed COLX, RUNX2 and Matrilin-1, whereas the pellets from CPCs did not	McCarthy et al. (2012)
Human	47–71 years old (N = 51)		Knee articular cartilage	Normal looking OA cartilage	Dedifferentiated chondrocyte	Dedifferentiated chondrocytes showed similar properties as BMSC but showed higher chondrogenic potential, which could be used for cartilage repair	Jiang et al. (2016)
Human	56–68 years (N = 3)	Female	Knee articular cartilage	Normal looking OA cartilage	Fibronectin attachment	OA-CPC showed 1/12 TGFBR1 compared with OAC, resulting different effect of TGFb on OA-CPC and OAC.	Liu et al. (2020b)
Human	18 years (N = 1)	Female	Cell line	Normal cartilage	Fibronectin attachment	OA-CPC expressed high SHH that could induce OA-CPC proliferation, chondrogenesis, hypertrophy, and replicative senescence and could suppress COL2A1, stimulate MMP13, and induces apoptosis in OAC.	Feng et al. (2021)
	68 ± 1.6 years (N = 18)	13 M/5 F	Cell lines and primary CPCs from normal looking knee articular cartilage	Normal looking OA cartilage
Human	32–89 years old (N = 18)		Lateral femoral condyles cartilage	Normal cartilage	A mixture of chondrocyte and CPCs	CD10, CD90, CD105, CD166 were upregulated in OA chondrocyte during monolayer culture	Diaz-Romero et al. (2005)
Human	53.67 ± 5.9 years (N = 3)	1 M/2 F	Knee articular cartilage	Grade 4 OA cartilage	Fibronectin attachment	Fibronectin attached CPCs exhibited lower levels of hypertrophy markers (RUNX2 and COL10A1) compared with non-attached cells and total cells in OA cartilage	Kachroo et al. (2020)
Bovine	7 days		Metacarpophalangeal joints	Normal cartilage	Fibronectin attachment	Clonal CPCs could maintain telomerase activity and Sox9 expression after long time culture	Khan et al. (2009)
Human	10–57 years old (N = 9)		Femur condyle cartilage	Normal cartilage	Fibronectin attachment	Clonal CPCs showed longer telomere length and stronger telomerase activity than chondrocyte	Williams et al. (2010)
Caprine	Young and mature (N = 3)	Female	Lateral femoral condyle cartilage	Cartilage defect		CPCs combined with type I/III collagen membrane were used for cartilage defect
Bovine			Lateral tibial plateau cartilage	4-mm-diameter defects with 2-mm depth	Ex vivo	Short-term enzymatic treatment could activate CPCs migration, which may benefit cartilage repair	Schminke and Miosge (2014)
Human	65–75 years old		Adjacent to the main defect	OA cartilage	Migration	CPCs in late OA showed strong migration capacity. Knockdown RUNX2 could enhance SOX9 and aggrecan	Koelling et al. (2009)
Human	55 ± 4 years (N = 3)		Knee articular cartilage	Grade 4 OA cartilage	Migration or fibronectin attachment	Migratory CPC: lower levels of hypertrophy markers (RUNX2 and COL1A1), higher levels of chondrogenic markers (Aggrecan and COL2A1/COL1A1 ratio)	Vinod et al. (2021)
Bovine	15–24 months old		Tibial plateau cartilage	Normal cartilage	Blunt impact or scratch stimulated migration	CPCs were more sensitive to chemotaxis, cell lysates, condition medium and HMGB-1 than chondrocytes	Seol et al. (2012)
Human	29, 34, and 46 years old (N = 3)	Male
Human	45–87 years old (N = 71)		Knee articular cartilage	Non-fibrillated regions	Migration	PDGF or IGF-1 stimulated CPCs migration, which could be abolished by IL-1b or TNFa but not IL-6	Joos et al. (2013)
Bovine			Tibial plateaus	Normal cartilage	Migration	CPCs showed phagocytic capacity when injury happened	Zhou et al. (2016)