Table 2 Summary of the biological function of the oral tissue stem cells derived exosomes

Immunomodulatory effects

DPSCs-Exos

Inhibit differentiation of CD4 + T cells into Th17

Reduce secretion of pro-inflammatory factors IL-17, TNF-α

Promote polarization of CD4 + T cells into Treg cells

Increase release of anti-inflammatory factors IL-10, TGF-β

[39, 40, 43]

SHEDs-Exos

Suppress the expression of IL-6, IL-8, MMP1, MMP3, MMP9, MMP13, and ADAMTS5

SHEDs-Exo-enriched miR-100 suppresses inflammation via repression of mammalian target of rapamycin

Suppressed carrageenan-induced acute inflammation in mice and suppressed the activities of cathepsin B and MMPs at the site of acute inflammation

Low doses of exosomes inhibited the expression of the inflammatory cytokines IL-6 and TNF-α

Osteogenesis effects

SCAPs-Exos

Enriched osteogenesis promoted pi-RNAs target to MAPK pathway

[41,42,43,44,45]

SHEDs-Exos

High ALP activity and upregulated osteogenic gene expression, including: RUNX2, OPN and OCN

Contained the mRNA and proteins of Wnt3a and BMP2 activated BMP/Smad and Wnt/β-catenin signaling pathways

Inhibit the apoptosis of BMSCs, promote the RUNX2 and p-Smad5 expression

Inhibited adipogenesis

GMSCs-Exos

Promote the expression of osteogenic markers: RUNX2, VEGFA OPN and COL1A1

Combine the exosomes with the biomaterials promoted the formation of new bone spicules and blood vessels in the rat model

Odontogenic effects

DPSCs-Exos

Upregulation of DSP, DMP-1, ALP, and RUNX2, downregulation of latent TGF-β-binding protein 1

Promoted odontogenic differentiation via the TGFβ1/Smad signaling pathway

Triggered the P38/MAPK pathway and promoted the expression of the genes required for odontogenic differentiation, including DMP1 and DPP

Modulate Schwann Cells migration and odontogenic differentiation

Attenuated the LPS-induced cell apoptosis of odontoblast-like cells

[33, 46, 47, 49, 50]

SCAPs-Exos

Increased the gene expression of the dentinogenic marker DSP

Promoted BMMSCs-based dentine-pulp complex regeneration

Neuroprotection and nerve regeneration

DPSCs-Exos

Protected neurons against excitotoxicity in vitro via the activation of endogenous cell survival mechanisms

Upregulate the host's endogenous growth factor expression and prevent apoptosis via activation of the cell survival PI3K-B-cell lymphoma-2 pathway

[32, 37, 52,53,54,55,56]

SHEDs-Exos

Suppressed 6-OHDA-induced gait impairments and slowed the number of 6-OHDA-induced contralateral rotations

Significantly inhibited the secretion of TNF-α and IL-6

Reduce neuroinflammation by shifting microglia M1/M2 polarization

GMSCs-Exos

Promoted Schwann cell proliferation, migration and dorsal root ganglion axon growth

Increase in the expression of Notch1, c-JUN, GFAP, and SOX2

Combined with the biomaterials effectively promoted tongue taste bud regeneration and peripheral nerve regeneration

Wound healing and skin regeneration

GMSCs-Exos

Promote the re-epithelialization, deposition and remodeling of collagen and the enhancing of angiogenesis and neuronal ingrowth in the wound area

Contain higher amounts of IL-1RA

[57, 58]

Angiogenic effects

GMSCs-Exos

Contain exosomal miR-210 and promoted the expression of VEGF

[45, 59, 60]

DPSCs-Exos

HIF-1 enhanced exosomes secretion and increased the packaging of Jagged1

The addition of Jagged1-containing exosomes cultures to endothelial cells triggered transcriptional changes in Notch target genes and induced angiogenesis

Antitumor effects

GMSCs-Exos

PTX was incorporated into GMSCs-Exos during their biogenesis

Exosomes with PTX produced a significant dose-dependent inhibition of squamous cancer cell growth

[35, 62, 64]

DPSCs-Exos

After the transduction of DPSCs with the yCD::UPRT gene via retrovirus infection, the suicide gene yCD::UPRT mRNA was packed into the exosomes cargo

The exosomes were internalized via recipient tumor cells and effectively triggered dose-dependent tumor cell death in the presence of the prodrug 5-fluorocytosine