The role of fibroblasts in the modulation of dental pulp inflammation

The dental pulp can be affected by thermal, physical, chemical, and bacterial phenomena that stimulate the inflammatory response. The pulp tissue produces an immunological, cellular, and vascular reaction in an attempt to defend itself and resolve the affected tissue. The expression of different microRNAs during pulp inflammation has been previously documented. MicroRNAs (miRNAs) are endogenous small molecules involved in the transcription of genes that regulate the immune system and the inflammatory response. They are present in cellular and physiological functions, as well as in the pathogenesis of human diseases, becoming potential biomarkers for diagnosis, prognosis, monitoring, and safety. Previous studies have evidenced the different roles played by miRNAs in proinflammatory, anti-inflammatory, and immunological phenomena in the dental pulp, highlighting specific key functions of pulp pathology. This systematized review aims to provide an understanding of the role of the different microRNAs detected in the pulp and their effects on the expression of the different target genes that are involved during pulp inflammation.

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Immunomodulatory Expression of Cathelicidins Peptides in Pulp Inflammation and Regeneration: An Update

Current Issues in Molecular Biology ◽

10.3390/cimb43010010 ◽

2021 ◽

Vol 43 (1) ◽

pp. 116-126

Author(s):

Nireeksha ◽

Sudhir Rama Varma ◽

Marah Damdoum ◽

Mohammed Amjed Alsaegh ◽

Mithra N. Hegde ◽

...

Keyword(s):

Cell Differentiation ◽

Dental Pulp ◽

Secretory Activity ◽

Local Environment ◽

Innate Immune ◽

Reparative Dentin ◽

Pulp Inflammation ◽

Dentin Formation ◽

Immunomodulatory Potential

The role of inflammatory mediators in dental pulp is unique. The local environment of pulp responds to any changes in the physiology that are highly fundamental, like odontoblast cell differentiation and other secretory activity. The aim of this review is to assess the role of cathelicidins based on their capacity to heal wounds, their immunomodulatory potential, and their ability to stimulate cytokine production and stimulate immune-inflammatory response in pulp and periapex. Accessible electronic databases were searched to find studies reporting the role of cathelicidins in pulpal inflammation and regeneration published between September 2010 and September 2020. The search was performed using the following databases: Medline, Scopus, Web of Science, SciELO and PubMed. The electronic search was performed using the combination of keywords “cathelicidins” and “dental pulp inflammation”. On the basis of previous studies, it can be inferred that LL-37 plays an important role in odontoblastic cell differentiation and stimulation of antimicrobial peptides. Furthermore, based on these outcomes, it can be concluded that LL-37 plays an important role in reparative dentin formation and provides signaling for defense by activating the innate immune system.

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Resolvin E1 accelerates pulp repair by regulating inflammation and stimulating dentin regeneration in dental pulp stem cells

Stem Cell Research & Therapy ◽

10.1186/s13287-021-02141-y ◽

2021 ◽

Vol 12 (1) ◽

Author(s):

Jie Chen ◽

Huaxing Xu ◽

Kun Xia ◽

Shuhua Cheng ◽

Qi Zhang

Keyword(s):

Dental Pulp ◽

Tissue Repair ◽

Pulp Tissue ◽

Tissue Repair And Regeneration ◽

Injury Model ◽

Tnf Α ◽

Pulp Inflammation ◽

Inflammation Resolution ◽

Pulp Repair ◽

Dentin Regeneration

Abstract Background Unresolved inflammation and tissue destruction are considered to underlie the failure of dental pulp repair. As key mediators of the injury response, dental pulp stem cells (DPSCs) play a critical role in pulp tissue repair and regeneration. Resolvin E1 (RvE1), a major dietary omega-3 polyunsaturated fatty-acid metabolite, is effective in resolving inflammation and activating wound healing. However, whether RvE1 facilitates injured pulp-tissue repair and regeneration through timely resolution of inflammation and rapid mobilization of DPSCs is unknown. Therefore, we established a pulp injury model and investigated the effects of RvE1 on DPSC-mediated inflammation resolution and injured pulp repair. Methods A pulp injury model was established using 8-week-old Sprague-Dawley rats. Animals were sacrificed on days 1, 3, 7, 14, 21, and 28 after pulp capping with a collagen sponge immersed in PBS with RvE1 or PBS. Hematoxylin-eosin and Masson’s trichrome staining, immunohistochemistry, and immunohistofluorescence were used to evaluate the prohealing properties of RvE1. hDPSCs were incubated with lipopolysaccharide (LPS) to induce an inflammatory response, and the expression of inflammatory factors after RvE1 application was measured. Effects of RvE1 on hDPSC proliferation, chemotaxis, and odontogenic differentiation were evaluated by CCK-8 assay, transwell assay, alkaline phosphatase (ALP) staining, alizarin red staining, and quantitative PCR, and possible signaling pathways were explored using western blotting. Results In vivo, RvE1 reduced the necrosis rate of damaged pulp and preserved more vital pulps, and promoted injured pulp repair and reparative dentin formation. Further, it enhanced dentin matrix protein 1 and dentin sialoprotein expression and accelerated pulp inflammation resolution by suppressing TNF-α and IL-1β expression. RvE1 enhanced the recruitment of CD146+ and CD105+ DPSCs to the damaged molar pulp mesenchyme. Isolated primary cells exhibited the mesenchymal stem cell immunophenotype and differentiation. RvE1 promoted hDPSC proliferation and chemotaxis. RvE1 significantly attenuated pro-inflammatory cytokine (TNF-α, IL-1β, and IL-6) release and enhanced ALP activity, nodule mineralization, and especially, expression of the odontogenesis-related genes DMP1, DSPP, and BSP in LPS-stimulated DPSCs. RvE1 regulated AKT, ERK, and rS6 phosphorylation in LPS-stimulated DPSCs. Conclusions RvE1 promotes pulp inflammation resolution and dentin regeneration and positively influences the proliferation, chemotaxis, and differentiation of LPS-stimulated hDPSCs. This response is, at least partially, dependent on AKT, ERK, and rS6-associated signaling in the inflammatory microenvironment. RvE1 has promising application potential in regenerative endodontics.

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NLRP6‐caspase 4 inflammasome activation in response to cariogenic bacterial lipoteichoic acid in human dental pulp inflammation

International Endodontic Journal ◽

10.1111/iej.13469 ◽

2020 ◽

Author(s):

X. Tian ◽

R. Li ◽

C. Liu ◽

F. Liu ◽

L.J. Yang ◽

...

Keyword(s):

Dental Pulp ◽

Lipoteichoic Acid ◽

Inflammasome Activation ◽

Pulp Inflammation ◽

Human Dental Pulp

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Role of CTGF/CCN2 in reparative dentinogenesis in human dental pulp

Journal of Oral Science ◽

10.2334/josnusd.54.47 ◽

2012 ◽

Vol 54 (1) ◽

pp. 47-54 ◽

Cited By ~ 7

Author(s):

Koichiro Muromachi ◽

Naoto Kamio ◽

Takashi Matsumoto ◽

Kiyoshi Matsushima

Keyword(s):

Dental Pulp ◽

Human Dental Pulp

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Reactionary Versus Reparative Dentine in Deep Caries

ARS Medica Tomitana ◽

10.2478/arsm-2019-0004 ◽

2019 ◽

Vol 25 (1) ◽

pp. 15-21

Author(s):

Iliescu Alexandru-Andrei ◽

Gheorghiu Irina-Maria ◽

Tănase Mihaela ◽

Iliescu Andrei ◽

Mitran Loredana ◽

...

Keyword(s):

Stem Cells ◽

Dental Pulp ◽

Dental Pulp Stem Cells ◽

Complex Response ◽

Pulp Inflammation ◽

Proliferation And Differentiation ◽

Molecular Signals

Abstract The dentine-pulp complex response in deep caries is histological characterized by tertiary formation and mild chronic pulp inflammation. The quiescent primary odontoblasts are reactivated, laying down reactionary tertiary dentine. In more severe carious damage the primary odontoblasts die and reparative tertiary dentine is secreted by odontoblast-like cells, which are differentiated in adult teeth mainly from dental pulp stem cells DPSC. Though associated with reversible pulpitis DPSC still preserve in deep caries the capability of migration, proliferation and differentiation. Some common mechanisms of molecular signals involved in tertiary dentine formation might also explain the balance between inflammation and regeneration of dentine-pulp complex.

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Sclerostin promotes human dental pulp cells senescence

PeerJ ◽

10.7717/peerj.5808 ◽

2018 ◽

Vol 6 ◽

pp. e5808 ◽

Cited By ~ 4

Author(s):

Yanjing Ou ◽

Yi Zhou ◽

Shanshan Liang ◽

Yining Wang

Keyword(s):

Dental Pulp ◽

Wnt Signaling Pathway ◽

Dental Pulp Cells ◽

Differentiation Potential ◽

Human Dental Pulp Cells ◽

Qrt Pcr ◽

Odontoblastic Differentiation ◽

Human Dental Pulp ◽

Pulp Cells

Background Senescence-related impairment of proliferation and differentiation limits the use of dental pulp cells for tissue regeneration. Deletion of sclerostin improves the dentinogenesis regeneration, while its role in dental pulp senescence is unclear. We investigated the role of sclerostin in subculture-induced senescence of human dental pulp cells (HDPCs) and in the senescence-related decline of proliferation and odontoblastic differentiation. Methods Immunohistochemical staining and qRT-PCR analyses were performed to examine the expression pattern of sclerostin in young (20–30-year-old) and senescent (45–80-year-old) dental pulps. HDPCs were serially subcultured until senescence, and the expression of sclerostin was examined by qRT-PCR analysis. HDPCs with sclerostin overexpression and knockdown were constructed to investigate the role of sclerostin in HDPCs senescence and senescence-related impairment of odontoblastic differentiation potential. Results By immunohistochemistry and qRT-PCR, we found a significantly increased expression level of sclerostin in senescent human dental pulp compared with that of young human dental pulp. Additionally, elevated sclerostin expression was found in subculture-induced senescent HDPCs in vitro. By sclerostin overexpression and knockdown, we found that sclerostin promoted HDPCs senescence-related decline of proliferation and odontoblastic differentiation potential with increased expression of p16, p53 and p21 and downregulation of the Wnt signaling pathway. Discussion The increased expression of sclerostin is responsible for the decline of proliferation and odontoblastic differentiation potential of HDPCs during cellular senescence. Anti-sclerostin treatment may be beneficial for the maintenance of the proliferation and odontoblastic differentiation potentials of HDPCs.

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