Document Type : Original Article

Author

Department of Orthodontics, Affiliated Hospital of Tangshan Vocational and Technical College, Tangshan, Hebei Province, 630000, China.

Abstract

Background: Periodontitis is a persistent inflammatory condition that impacts the tissues supporting the teeth, ultimately causing tooth loss. Recent research indicates that mesenchymal stem cells (MSCs) and their extracellular vesicles (EVs) play a crucial role in periodontitis by modulating the activities of cells in the gums, the immune system, and the surrounding area.
Objective: To investigate the therapeutic potential of human umbilical cord mesenchymal stem cells (hUCSCs) and EVs in modulating the inflammatory response associated with periodontitis.
Methods: hUCSCs were isolated, subjected to flow cytometry analysis of surface markers, and differentiated into adipocyte and osteocyte. hUCSC-EVs were isolated and characterized using flow cytometry and electron microscopy. A periodontitis animal model was established in 30 female C57Bl/6 mice by inducing ligature-induced inflammation. After two weeks, experimental groups received hUCSCs or hUCSCs-EVs, or vehicles intravenously. Animals were monitored for 4 weeks, and the periodontal tissues were used to investigate the impacts of hUCSCs and hUCSCs-EVs on the expression of pro- (TNF-α, IFN-γ, and IL-17a) and anti- (TGF-β, IL-10, and IL-4) inflammatory cytokines by real-time PCR. The secretion of these cytokines by splenocytes was also evaluated by ELISA.
Results: Our findings revealed that the levels of IL-17a, IFN-γ, and TNFα significantly reduced, while TGF-β and IL-10 significantly elevated in the periodontal tissues of the hUCSC and hUCSC-EVs-treated mice compared with the controls. Furthermore, the expression of TNF-α, IFN-γ, and IL-17a significantly decreased, while the production of IL-10 and TGF-β significantly increased in splenocytes from the hUCSC and EVs-treated mice.
Conclusion: hUCSCs and their EVs have the potential to attenuate the inflammatory response associated with periodontitis. This effect could potentially be exerted through the downregulation of pro-inflammatory cytokines and the upregulation of anti-inflammatory ones.

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