Xixi Wang
Abstract
Background: Periodontitis is a chronic inflammatory condition that affects the tissues supporting the teeth, ultimately leading to tooth loss. Mesenchymal stem cells (MSCs) and their extracellular vesicles (EVs) play a crucial role in periodontitis by modulating the activities of gum cells and the immune ...
Read More
Background: Periodontitis is a chronic inflammatory condition that affects the tissues supporting the teeth, ultimately leading to tooth loss. Mesenchymal stem cells (MSCs) and their extracellular vesicles (EVs) play a crucial role in periodontitis by modulating the activities of gum cells and the immune system.Objective: To investigate the therapeutic potential of human umbilical cord mesenchymal stem cells (hUCSCs) and EVs in regulating 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. Experimental groups received hUCSCs or hUCSCs-EVs, or vehicles intravenously. Animals were monitored for 4 weeks, and the periodontal tissues were used to assess the effects of hUCSCs and hUCSCs-EVs on the expression of pro- (TNF-α, IFN-γ, and IL-17a) and anti-inflammatory cytokines (TGF-β, IL-10, and IL-4). The secretion of these cytokines by splenocytes was also evaluated using ELISA.Results: The levels of IL-17a, IFN-γ, and TNFα significantly reduced, while TGF-β and IL-10 significantly increased in the periodontal tissues of the hUCSC and hUCSCEVs-treated mice. 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, possibly by downregulating pro-inflammatory cytokines and upregulating anti-inflammatory ones.
Mandana Sattari; Alireza Fathiyeh; Fatemeh Gholami; Hassan Darbandi Tamijani; Mahdi Ghatreh Samani
Volume 8, Issue 1 , March 2011, , Pages 20-26
Abstract
Background: Growth factors play a major part in wound healing in many tissues including the periodontium. Transforming growth factor-β1 (TGF-β1) is one of these factors present in the gingival crevicular fluid. In addition, it is considered as one of the most important anti-inflammatory cytokines. ...
Read More
Background: Growth factors play a major part in wound healing in many tissues including the periodontium. Transforming growth factor-β1 (TGF-β1) is one of these factors present in the gingival crevicular fluid. In addition, it is considered as one of the most important anti-inflammatory cytokines. Interleukin-1β is a proinflammatory cytokine that presents itself in gingival inflammation and the GCF. Such factors might be of value as prognostic markers of wound healing activity and the therapeutic progress following flap surgery. Objective: The aim of this study was to evaluate the effect of surgical flap on the concentration of IL-1β and TGF-β in the GCF of patients with moderate to severe chronic periodontitis. Methods: The GCF samples were collected, using the Perio-Paper strip at phase 1 (pre-surgery), phase 2 (4th week post surgery) and phase 3 (12th week post surgery) from 20 sites of 10 patients undergoing flap surgery. After the elution, IL-1β and TGF-β concentrations were measured by enzyme-linked immunosorbent assay (ELISA). Results: The mean TGF-β and IL-1β concentration decreased from phase 1 to phase 3 (p<0.05). There were no significant statistical correlations between IL-1β and TGF-β1 concentrations in the 3 assessment phases. There was a significant statistical correlation between TGF-β1 concentrations and the Plaque Index (PI) in phase 2 (p<0.05). There was a significant statistical correlation (p<0.05) between IL-1β and TGF-β1 concentration and the probing pocket depth (PPD). Conclusion: The flap surgery has a significant effect on decreasing IL-1β concentration. In the case of TGF-β1, probably the decrease in the concentration after treatment might be due to the removal of the inflammatory stimulants.
Mehrdad Radvar; Jalil Tavakkol-Afshari; Mahboobeh N. Bajestan; Mohammad-Reza Naseh; Hamid-Reza Arab
Abstract
Background: Several cytokines, including IL-6 have been implicated in the pathogenesis of periodontal disease. It is established that monocytes from periodontitis subjects show an increased production of IL-6 as compared to healthy subjects. However, little is known about the effect of periodontal ...
Read More
Background: Several cytokines, including IL-6 have been implicated in the pathogenesis of periodontal disease. It is established that monocytes from periodontitis subjects show an increased production of IL-6 as compared to healthy subjects. However, little is known about the effect of periodontal treatment on IL-6 production by monocytes in subsets of periodontitis patients. Objective: The aim of the present study was to evaluate the effect of surgical periodontal treatment on IL-6 production of peripheral blood monocytes (PBM) in aggressive periodontitis patients (AP) and chronic periodontitis patients (CP) before and after stimulation by E.coli LPS. Methods: Fifteen AP patients, 15 CP patients and 15 periodontally healthy subjects (PH) took part in the study. PBM IL-6 pro-duction was measured, using ELISA, before and after stimulation of cultured PBM cells by 0.1 microg/ml LPS of E.coli. Following full-mouth non-surgical and surgical periodontal treatment of the AP and CP groups, the same measurements were repeated for these two groups. Results: LPS-stimulated IL-6 production was significantly greater than non-stimulated IL-6 for all 3 groups. Before periodontal treatment, LPS-stimulated IL-6 pro-duction of the AP group was significantly greater than the other 2 groups. Periodontal treatment did not result in a significant decrease in unstimulated or LPS-stimulated IL-6 production by PBM cells in AP and CP patients. No correlation was detected between IL-6 levels and baseline clinical parameters or changes in clinical parameters. Conclusion: PBM cells in AP patients might be hyper-responsive in terms of IL-6 production. This hyper-responsiveness does not seem to return to that of healthy subjects even after a successful periodontal treatment. Moreover, the regulation of host inflammatory mechanisms upon LPS challenge might be different between AP and CP patients.
