Table 2.

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

Biological effects	Type of exosomes	Mechanism	References
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	[41–45]
	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, 52–56]
	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