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Molecular Advances in Dental Pulp Tissue Engineering, 2nd Edition
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Molecular Advances in Dental Pulp Tissue Engineering, 2nd Edition

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Materials Science".

Deadline for manuscript submissions: 20 February 2025 | Viewed by 5012

Special Issue Editors

Prof. Dr. Matthias Widbiller

E-Mail Website
Guest Editor
Department of Conservative Dentistry and Periodontology, University Hospital Regensburg, Franz-Josef-Strauß-Allee 11, D-93093 Regensburg, Germany
Interests: pulp biology; tissue engineering; dentin matrix proteins; dental pulp stem cells
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Kerstin M. Galler

E-Mail Website
Guest Editor
Department of Operative Dentistry and Periodontology, Friedrich-Alexander-University Erlangen-Nuernberg, D-91054 Erlangen, Germany
Interests: pulp biology; tissue engineering; scaffold materials; dental pulp stem cells

Special Issue Information

Dear Colleagues,

Protected by the surrounding mineralized barriers, such as enamel, dentin and cementum, dental pulp is a functionally versatile tissue that fulfils various tasks. Besides the perception of thermal and mechanical stimuli as a warning system as well as the deposition of dentin, the pulp exerts a variety of immunological functions, in terms of both recognition and of defense. In young patients, a sound and functional dental pulp is indispensable for the completion of root development, and early pulp necrosis results in fracture-prone teeth with fragile root walls. Whether in young or adult patients, the loss of pulp tissue after caries or trauma requires therapeutic intervention by root canal treatment and filling with a synthetic material, which results in the loss of all its physiological functions.

In recent years, creative and multi-faceted attempts have been made to regenerate this valuable tissue using advanced molecular biology methods. Promising approaches based on tissue engineering and regenerative medicine (TERM) have been developed for this purpose. These stem-cell-based or primarily cell-free procedures use specifically customized scaffold materials and biologically active molecules to achieve true regeneration of the dental pulp in terms of both its architecture and function. Several of these approaches are already taking requirements for clinical application into consideration.

This Special Issue aims to present the scientific progress in this field of research. The goal is to collect innovative studies in the field of stem cell biology, scaffold material development or molecular signaling that contribute to the transfer of this knowledge from the bench to the dental clinic.

More published papers could be found in the closed Special Issue: Molecular Advances in Dental Pulp Tissue Engineering.

Prof. Dr. Matthias Widbiller
Prof. Dr. Kerstin M. Galler
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • tissue engineering and regenerative medicine (TERM)
  • pulp regeneration
  • scaffold materials
  • stem cells
  • bioactive molecules
  • dentin matrix proteins

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Published Papers (4 papers)

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Research

10 pages, 1208 KiB  
Communication
Investigation of Angiogenic Potential in CD146-Positive Stem Cells Derived from Human Exfoliated Deciduous Teeth
by Kodai Rikitake, Ryo Kunimatsu, Yuki Yoshimi and Kotaro Tanimoto
Int. J. Mol. Sci. 2025, 26(3), 974; https://doi.org/10.3390/ijms26030974 - 24 Jan 2025
Viewed by 295
Abstract
This study aimed to evaluate the effects of CD146, a surface antigen of mesenchymal stem cells from human exfoliated deciduous teeth (SHEDs), on angiogenic potential. SHEDs were isolated from patients’ deciduous teeth and sorted into CD146-positive (CD146 + SHED) and CD146-negative (CD146 − [...] Read more.
This study aimed to evaluate the effects of CD146, a surface antigen of mesenchymal stem cells from human exfoliated deciduous teeth (SHEDs), on angiogenic potential. SHEDs were isolated from patients’ deciduous teeth and sorted into CD146-positive (CD146 + SHED) and CD146-negative (CD146 − SHED) populations. Three groups—non-sorted SHED, CD146 + SHED, and CD146 − SHED—were compared. Angiogenic potential was assessed by co-culturing each group with human umbilical vein endothelial cells (HUVECs) and evaluating lumen formation using an endothelial tube formation assay. The gene and protein expression levels of angiogenic markers, including vascular endothelial growth factor (VEGF), VEGF receptor 2 (VEGFR2), cluster of differentiation 31 (CD31), and basic fibroblast growth factor (bFGF), were analyzed using a real-time polymerase chain reaction and enzyme-linked immunosorbent assay. The tube formation assay revealed significantly enhanced angiogenic potential in CD146 + SHED and non-sorted SHED compared to CD146 − SHED. The gene and protein expression levels of VEGF, VEGFR2, CD31, and bFGF were significantly upregulated in CD146 + SHED and non-sorted SHED, highlighting superior angiogenic capabilities in CD146 + SHED. CD146 + SHED demonstrated enhanced angiogenic potential compared to CD146 − SHED, supporting their use in regenerative therapies targeting angiogenesis. Full article
(This article belongs to the Special Issue Molecular Advances in Dental Pulp Tissue Engineering, 2nd Edition)
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14 pages, 2183 KiB  
Article
Small Extracellular Vesicles Derived from Lipopolysaccharide-Treated Stem Cells from the Apical Papilla Modulate Macrophage Phenotypes and Inflammatory Interactions in Pulpal and Periodontal Tissues
by Solène Tessier, Boris Halgand, Davy Aubeux, Joëlle Véziers, Angélique Galvani, Juliette Jamoneau, Fabienne Pérez, Valérie Geoffroy and Alexis Gaudin
Int. J. Mol. Sci. 2025, 26(1), 297; https://doi.org/10.3390/ijms26010297 - 31 Dec 2024
Viewed by 634
Abstract
Inflammation significantly influences cellular communication in the oral environment, impacting tissue repair and regeneration. This study explores the role of small extracellular vesicles (sEVs) derived from lipopolysaccharide (LPS)-treated stem cells from the apical papilla (SCAP) in modulating macrophage polarization and osteoblast differentiation. SCAPs [...] Read more.
Inflammation significantly influences cellular communication in the oral environment, impacting tissue repair and regeneration. This study explores the role of small extracellular vesicles (sEVs) derived from lipopolysaccharide (LPS)-treated stem cells from the apical papilla (SCAP) in modulating macrophage polarization and osteoblast differentiation. SCAPs were treated with LPS for 24 h, and sEVs from untreated (SCAP-sEVs) and LPS-treated SCAP (LPS-SCAP-sEVs) were isolated via ultracentrifugation and characterized using transmission electron microscopy, Western blot, and Tunable Resistive Pulse Sensing. LPS-SCAP-sEVs exhibited characteristic exosome morphology (~100 nm diameter) and expressed vesicular markers (CD9, CD63, CD81, and HSP70). Functional analysis revealed that LPS-SCAP-sEVs promoted M1 macrophage polarization, as evidenced by the increased pro-inflammatory cytokines (IL-6 and IL-1β) and the reduced anti-inflammatory markers (IL-10 and CD206), while impairing the M2 phenotype. Additionally, LPS-SCAP-sEVs had a minimal impact on SCAP metabolic activity or osteogenic gene expression but significantly reduced mineralization capacity in osteogenic conditions. These findings suggest that sEVs mediate the inflammatory interplay between SCAP and macrophages, skewing macrophage polarization toward a pro-inflammatory state and hindering osteoblast differentiation. Understanding this sEV-driven communication axis provides novel insights into the cellular mechanisms underlying inflammation in oral tissues and highlights potential therapeutic targets for modulating extracellular vesicle activity during acute inflammatory episodes. Full article
(This article belongs to the Special Issue Molecular Advances in Dental Pulp Tissue Engineering, 2nd Edition)
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16 pages, 16192 KiB  
Article
Impaired Tertiary Dentin Secretion after Shallow Injury in Tgfbr2-Deficient Dental Pulp Cells Is Rescued by Extended CGRP Signaling
by Monica Stanwick, Fatma Fenesha, Ahmed Hamid, Khushroop Kang, Dane Kanniard, Irene Kim, Nicholas Mandarano, Fernanda L. Schumacher and Sarah B. Peters
Int. J. Mol. Sci. 2024, 25(13), 6847; https://doi.org/10.3390/ijms25136847 - 21 Jun 2024
Viewed by 1499
Abstract
The transforming growth factor β (TGFβ) superfamily is a master regulator of development, adult homeostasis, and wound repair. Dysregulated TGFβ signaling can lead to cancer, fibrosis, and musculoskeletal malformations. We previously demonstrated that TGFβ receptor 2 (Tgfbr2) signaling regulates odontoblast differentiation, [...] Read more.
The transforming growth factor β (TGFβ) superfamily is a master regulator of development, adult homeostasis, and wound repair. Dysregulated TGFβ signaling can lead to cancer, fibrosis, and musculoskeletal malformations. We previously demonstrated that TGFβ receptor 2 (Tgfbr2) signaling regulates odontoblast differentiation, dentin mineralization, root elongation, and sensory innervation during tooth development. Sensory innervation also modulates the homeostasis and repair response in adult teeth. We hypothesized that Tgfbr2 regulates the neuro-pulpal responses to dentin injury. To test this, we performed a shallow dentin injury with a timed deletion of Tgfbr2 in the dental pulp mesenchyme of mice and analyzed the levels of tertiary dentin and calcitonin gene-related peptide (CGRP) axon sprouting. Microcomputed tomography imaging and histology indicated lower dentin volume in Tgfbr2cko M1s compared to WT M1s 21 days post-injury, but the volume was comparable by day 56. Immunofluorescent imaging of peptidergic afferents demonstrated that the duration of axon sprouting was longer in injured Tgfbr2cko compared to WT M1s. Thus, CGRP+ sensory afferents may provide Tgfbr2-deficient odontoblasts with compensatory signals for healing. Harnessing these neuro-pulpal signals has the potential to guide the development of treatments for enhanced dental healing and to help patients with TGFβ-related diseases. Full article
(This article belongs to the Special Issue Molecular Advances in Dental Pulp Tissue Engineering, 2nd Edition)
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16 pages, 4952 KiB  
Article
Biological Effects of “Inflammageing” on Human Oral Cells: Insights into a Potential Confounder of Age-Related Diseases
by Elli Alexakou, Athina Bakopoulou, Danae A. Apatzidou, Aristeidis Kritis, Andigoni Malousi and Vassiliki Anastassiadou
Int. J. Mol. Sci. 2024, 25(1), 5; https://doi.org/10.3390/ijms25010005 - 19 Dec 2023
Cited by 2 | Viewed by 1799
Abstract
Objectives: The term “inflammageing” describes the process of inflammation-induced aging that leads living cells to a state of permanent cell cycle arrest due to chronic antigenic irritation. This in vitro study aimed to shed light on the mechanisms of “inflammageing” on human oral [...] Read more.
Objectives: The term “inflammageing” describes the process of inflammation-induced aging that leads living cells to a state of permanent cell cycle arrest due to chronic antigenic irritation. This in vitro study aimed to shed light on the mechanisms of “inflammageing” on human oral cells. Methods: Primary cultures of human gingival fibroblasts (hGFs) were exposed to variable pro-inflammatory stimuli, including lipopolysaccharide (LPS), Tumor Necrosis Factor-alpha (TNFa), and gingival crevicular fluid (GCF) collected from active periodontal pockets of systemically healthy patients. Inflammageing was studied through two experimental models, employing either late-passage (“aged”) cells (p. 10) that were exposed to the pro-inflammatory stimuli or early-passage (“young”) cells (p. 1) continuously exposed during a period of several passages (up to p. 10) to the above-mentioned stimuli. Cells were evaluated for the expression of beta-galactosidase activity (histochemical staining), senescence-associated genes (qPCR analysis), and biomarkers related to a Senescence-Associated Secretory Phenotype (SASP), through proteome profile analysis and bioinformatics. Results: A significant increase (p < 0.05) in beta-galactosidase-positive cells was observed after exposure to each pro-inflammatory stimulus. The senescence-associated gene expression included upregulation for CCND1 and downregulation for SUSD6, and STAG1, a profile typical for cellular senescence. Overall, pro-inflammatory priming of late-passage cells caused more pronounced effects in terms of senescence than long-term exposure of early-passage cells to these stimuli. Proteomic analysis showed induction of SASP, evidenced by upregulation of several pro-inflammatory proteins (IL-6, IL-10, IL-16, IP-10, MCP-1, MCP-2, M-CSF, MIP-1a, MIP-1b, TNFb, sTNF-RI, sTNF-RII, TIMP-2) implicated in cellular aging and immune responses. The least potent impact on the induction of SASP was provoked by LPS and the most pronounced by GCF. Conclusion: This study demonstrates that long-term exposure of hGFs to various pro-inflammatory signals induced or accelerated cellular senescence with the most pronounced impact noted for the late-passage cells. The outcome of these analyses provides insights into oral chronic inflammation as a potential confounder of age-related diseases. Full article
(This article belongs to the Special Issue Molecular Advances in Dental Pulp Tissue Engineering, 2nd Edition)
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