Table 2 The effects of CGF on SCS regeneration in DPC regeneration and its potential molecular mechanism

Hong et al. (2019) [18]

h-SCAPs

Proliferation, migration, and odonto/osteogenic differentiation

Cell counting kit-8;

Transwell Filter Inserts;

ARS and qPCR (ALP, DSPP, DMP-1)

CGF can significantly promote the proliferation, migration, and differentiation of SCAPs, and no dose-dependent manner effect.

More migration effect may be caused by the abundant chemotactic factors released from the CGF, including PDGF-BB and bFGF.

Hong et al. (2018) [34]

h-SCAPs

Proliferation, migration, and odonto/osteogenic differentiation

Cell counting kit-8;

Transwell assays;

ARS and qPCR (ALP, DSPP, DMP-1)

CGF can significantly promote the proliferation, migration, and differentiation of SCAPs, and no dose-dependent manner effect. CGF had an early inhibitory effect on the odonto/osteogenic differentiation of SCAPs.

The early inhibitory effect may be caused by proinflammatory factors such as TNF-α and IL-1 in CGF.

Xu et al. (2019) [35]

h-DPSCs exposed to LPS

Proliferation, migration, and odonto/osteogenic differentiation

Cell counting kit-8;

Transwell assays;

ALP activity, ARS, and qPCR (DMP-1, DSPP, OPN, RUNX2)

CGF promoted the proliferation, migration, and differentiation of DPSCs exposed to LPS in a dose-dependent manner.

The secretion of TNF-α and IL-8 in DPSCs treated by CGF could promote the DPSCs migration.

Tian et al. (2019) [36]

h-DPSCs

Proliferation, migration, and odonto/osteogenic differentiation

Cell counting kit-8;

Transwell assays;

ALP activity, ARS, and qPCR (DMP-1, DSPP, BSP, RUNX2)

CGF promoted the proliferation and migration of DPSCs in a dose-dependent manner, and CGF enhanced DPSCs odonto/osteogenic differentiation by upregulating RUNX2 transcription.

BMP-2/SMAD5/Runx2 signaling axis is related to CGF-mediated DPSCs mineralization.

Jin et al. (2018) [37]

h-DPSCs

Proliferation, migration, endothelial differentiation, and odontoblastic differentiation

Cell counting kit-8;

Scratches;

ALP activity, ARS, western blotting (VEGFR2, CD31), qRT-PCR (DMP-1, DSPP), and tube formation assay

CGF promoted the proliferation of DPSCs in a dose-dependent manner, and high concentrations of CGF inhibited the endothelial differentiation and odontoblastic differentiation of DPSCs.

The negative role of high-dosage CGF may be associated with the excess content of TGF-β, IL-1β, and IL-6 with increasing concentration.

Aghamohamadi et al. (2020) [38]

h-PDLSCs

Proliferation

MTT assay

CGF promoted PDLSCs proliferation in no dose-dependent manner, and high concentrations of CGF markedly inhibited the proliferation of PDLSCs

The high-dosage inhibition effect is thought to be mediated by TGF-β and proteolytic enzymes.

Li et al. (2019) [39]

h-PDLCs stimulated by TNF-α

Proliferation, osteogenic differentiation

Cell counting kit-8 assays;

ARS, ALP activity, western blotting, and qPCR (OCN, OSX, RUNX2)

CGF enhanced h-PDLCs proliferation and osteogenic differentiation in the presence of TNF-α-induced inflammation.

TGF-β1 contained in CGF relieved the inhibitory effect of TNF-α on the osteogenic differentiation of h-PDLCs by inducing the upregulation of Runx2 transcription.

Yu and Wang (2014) [40]

Beagle-PDLSCs

Proliferation, osteogenic differentiation

Cell counting and an MTT assay;

Mineralization nodule counts, ALP activity, western blotting, qPCR (BSP, OCN, COL1a1), and immunohistochemistry

CGF promoted PDLSCs proliferation and osteogenic differentiation in a time- and dose-dependent manner.

Rochira et al. (2020) [41]

h-BMSCs

Osteogenic differentiation

ALP activity, ARS, western blotting, qPCR (RUNX2, OSX, OPN, COL1a1)

CGF alone can induce osteogenic differentiation in h-BMSCs.

High RUNX2 expression and RUNX2 nuclear translocation are molecular mechanisms of h-BMSCs osteogenic differentiation induced by CGF.

Honda et al. (2013) [42]

hTERT-E6/E7 human MSCs

Proliferation, osteogenic differentiation

Cell counting;

ALP activity, ARS, western blotting, qPCR (RUNX2, OSX, OPN, COL1a1)

CGF, at concentrations between 1 and 10%, promoted proliferation, osteogenic maturation, and mineralization of hTERT-E6/E7 human MSCs in a dose-dependent manner, and higher concentrations of CGF had an inhibitory effect.