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The present study explored the effects of ascorbic-acid (AA)/retinol and timed inflammation on the stemness, the regenerative potential, and the transcriptomics profile of gingival mesenchymal stem/progenitor cells’ (G-MSCs). STRO-1 (mesenchymal stem cell marker) immuno-magnetically sorted G-MSCs were cultured in basic medium (control group), in basic medium with IL-1β (1 ng/mL), TNF-α (10 ng/mL) and IFN-γ (100 ng/mL, inflammatory-medium), in basic medium with AA (250 µmol/L) and retinol (20 µmol/L) (AA/retinol group) or in inflammatory medium with AA/retinol (inflammatory/AA/retinol group; <i>n</i> = 5/group). The intracellular levels of phosphorylated and total β-Catenin at 1 h, the expression of stemness genes over 7 days, the number of colony-forming units (CFUs) as well as the cellular proliferation aptitude over 14 days, and the G-MSCs’ multilineage differentiation potential were assessed. Next-generation sequencing was undertaken to elaborate on up-/downregulated genes and altered intracellular pathways. G-MSCs demonstrated all mesenchymal stem/progenitor cells characteristics. Controlled inflammation with AA/retinol significantly elevated <i>NANOG</i> (<i>p</i> < 0.05). The AA/retinol-mediated reduction in intracellular phosphorylated β-Catenin was restored through the effect of controlled inflammation (<i>p</i> < 0.05). Cellular proliferation was highest in the AA/retinol group (<i>p</i> < 0.05). AA/retinol counteracted the inflammation-mediated reduction in G-MSCs’ clonogenic ability and CFUs. Amplified chondrogenic differentiation was observed in the inflammatory/AA/retinol group. At 1 and 3 days, the differentially expressed genes were associated with development, proliferation, and migration (<i>FOS</i>, <i>EGR1</i>, <i>SGK1</i>, <i>CXCL5</i>, <i>SIPA1L2</i>, <i>TFPI2</i>, <i>KRATP1-5</i>), survival (<i>EGR1</i>, <i>SGK1</i>, <i>TMEM132A</i>), differentiation and mineral absorption (<i>FOS</i>, <i>EGR1</i>, <i>MT1E</i>, <i>KRTAP1-5</i>, <i>ASNS</i>, <i>PSAT1</i>), inflammation and MHC-II antigen processing (<i>PER1</i>, <i>CTSS</i>, <i>CD74</i>) and intracellular pathway activation (<i>FKBP5</i>, <i>ZNF404</i>). Less as well as more genes were activated the longer the G-MSCs remained in the inflammatory medium or AA/retinol, respectively. Combined, current results point at possibly interesting interactions between controlled inflammation or AA/retinol affecting stemness, proliferation, and differentiation attributes of G-MSCs.