Effects of sclerostin on lipopolysaccharide-induced inflammatory phenotype in human odontoblasts and dental pulp cells

Liao, Chufang; Ou, Yanjing; Wu, Yun; Zhou, Yi; Liang, Shanshan

doi:10.1016/j.biocel.2019.105628

Cited by 9 publications

(8 citation statements)

References 54 publications

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“…Upon LPS stimulation, production of sclerostin increased, impairing odontoblastic differentiation. Sclerostin activates NF-κB pathway, upregulating expression of IL-6, IL-8, IL-1β, ICAM-1, VCAM-1, CXCR4, MCP-1, VEGF, VEGFR-1 and PlGF [ 54 ].…”

Section: Resultsmentioning

confidence: 99%

Role of Lipopolysaccharide, Derived from Various Bacterial Species, in Pulpitis—A Systematic Review

et al. 2022

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Lipopolysaccharide (LPS) is widely used for induction of inflammation in various human tissues, including dental pulp. The purpose of this study was to summarize current medical literature focusing on (1) cell types used by researchers to simulate dental pulp inflammation, (2) LPS variants utilized in experimental settings and how these choices affect the findings. Our study was conducted in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA). We searched for studies reporting outcomes of lipopolysaccharide application on dental pulp cells in vitro using electronic databases: MEDLINE, Web of Science and Scopus. Having gathered data from 115 papers, we aimed to present all known effects LPS has on different cell types present in dental pulp. We focused on specific receptors and particles that are involved in molecular pathways. Our review provides an essential foundation for further research using in vitro models of pulpitis.

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Section: Resultsmentioning

confidence: 99%

Role of Lipopolysaccharide, Derived from Various Bacterial Species, in Pulpitis—A Systematic Review

et al. 2022

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“…DPCs, the most abundant cell types in dental pulp, are the main cells that function in host defenses and tissue regeneration in the pulp-dentin complex [ 18 ]. When exposed to bacteria and/or their toxic components, DPCs can recognize invading bacteria via their expression of a variety of pattern recognition receptors [ 1 , 19 – 21 ] and induce an innate immune response by expressing antimicrobial peptides (AMPs) and secreting various inflammatory cytokines, such as TNF-α, IL-6, IL-8, IL-1α, CCL7, CCL26, and CXCL11 [ 19 , 22 – 26 ], and these effects lead to the recruitment of macrophages, neutrophils, and other immune cells and initiation of the early inflammatory response to eliminate invading microbes [ 1 ].…”

Section: Discussionmentioning

confidence: 99%

Dental follicle stem cells rescue the regenerative capacity of inflamed rat dental pulp through a paracrine pathway

Hong

Chen

et al. 2020

Stem Cell Res Ther

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Background: Pulpitis is a common dental disease characterized by sustained inflammation and impaired pulp selfrepair. Mesenchymal stem cell-based minimally invasive vital pulp therapy (MSC-miVPT) is a potential treatment method, but its application is limited by the difficulty in acquiring MSCs. We recently revealed the immunomodulatory effects of rat dental follicle stem cells (rDFSCs) on acute lung injury. The present study focused on the paracrine effects of rDFSCs on the inflammation and regeneration of rat injured dental pulp to detect whether DFSCs are a potential candidate for MSC-miVPT. Methods: Conditioned medium from rDFSCs (rDFSC-CM) was applied to lipopolysaccharide (LPS)-induced inflammatory rat dental pulp cells (rDPCs). The inflammation and regeneration of rDPCs were detected by RT-qPCR, Western blotting, immunofluorescence staining, Cell Counting Kit-8 (CCK-8) assay, flow cytometry, wound-healing assay, and Masson's staining. The effects of rDFSC-CM on inflamed rat dental pulp were further evaluated by hematoxylin-eosin and immunohistochemical staining. Results: rDFSC-CM downregulated the ERK1/2 and NF-κB signaling pathways, which resulted in suppression of the expression of IL-1β, IL-6, and TNF-α and promotion of the expression of IL-4 and TGF-β, and these findings lead to the attenuation of rDPC inflammation. rDFSC-CM enhanced the in vitro proliferation, migration, and odontogenic differentiation of inflammatory rDPCs and their in vivo ectopic dentinogenesis. Furthermore, rDFSC-CM inhibited inflammatory cell infiltration in rat pulpitis and triggered Runx2 expression in some of the odontoblast-like cells surrounding the injured site, and these effects were conducive to the repair of inflamed dental pulp. Conclusions: rDFSC-CM exhibits therapeutic potential by rescuing the regeneration of the inflamed rat dental pulp through an immunomodulatory mechanism, indicating the application prospects of DFSCs in biological regenerative endodontics.

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“…In DPSCs, inflammatory cytokine interleukin-1β could downregulate sclerostin expression at the transcription level [57]. A previous in vitro study of the author found that in lipopolysaccharide-induced inflammatory condition, sclerostin promoted the production of several critical pro-inflammatory cytokines in odontoblasts and inhibited the odontoblastic differentiation of inflamed DPCs, revealing that sclerostin might play a pro-inflammatory role in dental pulp inflammation and impair dentin regeneration [55].…”

Section: Sclerostin and Pulp Inflammationmentioning

confidence: 96%

Sclerostin is a promising therapeutic target for oral inflammation and regenerative dentistry

et al. 2022

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Sclerostin is the protein product of the SOST gene and is known for its inhibitory effects on bone formation. The monoclonal antibody against sclerostin has been approved as a novel treatment method for osteoporosis. Oral health is one of the essential aspects of general human health. Hereditary bone dysplasia syndrome caused by sclerostin deficiency is often accompanied by some dental malformations, inspiring the therapeutic exploration of sclerostin in the oral and dental fields. Recent studies have found that sclerostin is expressed in several functional cell types in oral tissues, and the expression level of sclerostin is altered in pathological conditions. Sclerostin not only exerts similar negative outcomes on the formation of alveolar bone and bone-like tissues, including dentin and cementum, but also participates in the development of oral inflammatory diseases such as periodontitis, pulpitis, and peri-implantitis. This review aims to highlight related research progress of sclerostin in oral cavity, propose necessary further research in this field, and discuss its potential as a therapeutic target for dental indications and regenerative dentistry.

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Effects of sclerostin on lipopolysaccharide-induced inflammatory phenotype in human odontoblasts and dental pulp cells

Cited by 9 publications

References 54 publications

Role of Lipopolysaccharide, Derived from Various Bacterial Species, in Pulpitis—A Systematic Review

Role of Lipopolysaccharide, Derived from Various Bacterial Species, in Pulpitis—A Systematic Review

Dental follicle stem cells rescue the regenerative capacity of inflamed rat dental pulp through a paracrine pathway

Sclerostin is a promising therapeutic target for oral inflammation and regenerative dentistry

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