Effects of quercetin on human oral keratinocytes during re-epithelialization: An in vitro study

Abstract

Background: The width of keratinized mucosa plays an important role in esthetic and functional outcomes of dental implants. Lack of keratinized mucosa may lead to poor oral hygiene and greater soft-tissue recession. This study aimed at assessing the potential of quercetin in promoting human oral keratinocyte (HOK) proliferation and re-epithelialization in vitro.

Materials and methods: HOK were detected in the absence or presence of test substances. The Cell Counting Kit-8 was used to assess cell viability and proliferation capacity. Re-epithelization was assessed using a keratinocyte monolayer scratch assay. Cell migration was monitored via Transwell chambers. Porphyromonas gingivalis lipopolysaccharide was used to stimulate keratinocytes for mimicking the inflammatory situation. mRNA expression of inflammatory cytokines (interleukin-1beta, IL-1β and tumor necrosis factor alpha, TNF-α), cell adhesion molecules (Integrin-α6, Integrin-β4), and growth factors (transforming growth factor beta 1,TGF-β1 and transforming growth factor beta 3, TGF-β3) were estimated using RT-qPCR. Protein contents of TGF-β1 and TGF-β3 were investigated by enzyme-linked immunosorbent assay.

Results: Multiplex analysis revealed that quercetin enhances HOK proliferation via an upregulation of adhesion molecules (Integrin-α6β4). Additionally, re-epithelialization rate was significantly greater in the presence of quercetin than in the control (P < 0.01). Furthermore, 20 μM of quercetin increases both mRNA and protein levels of TGF-β3 under basal and wound conditions without affecting TGF-β1 production. Expressions of pro-inflammatory cytokines were downregulated by quercetin treatment.

Conclusion: Quercetin promotes HOKs proliferation and oral re-epithelialization in vitro.

Keywords: Oral keratinocytes; Quercetin; Re-epithelization; α6β4 integrin.