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Oral Inflammation—Environment, Molecules, and Cells in Oral Physiology and Pathology

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (31 December 2020) | Viewed by 56641

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Prof. Dr. Peter Proff

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Department of Orthodontics, Faculty of Medicine, University of Regensburg, Franz-Josef-Strauss-Allee 11, 93053 Regensburg, Germany
Interests: craniofacial development; orthodontic tooth movement; periodontal inflammation; oral immunology
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Special Issue Information

Dear Colleagues,

This Special Issue “Oral inflammation – Environment, Molecules, and Cells in Oral Physiology and Pathology” will cover a selection of recent research topics in the field of oral inflammation and immunology. Deciphering oral inflammatory processes and immune responses can advance our understanding of oral physiology and pathology, in general, with newly identified immune checkpoints being potential novel therapeutic targets for dental diseases and malformations.

The scope of this Special Issue, therefore, encompasses papers dealing with oral inflammation in etiopathogenesis and the clinical-biological manifestation of oral disease, malformations, and health with a focus on environment signals and molecules that can induce, shape, mediate, or propagate inflammatory conditions in the oral cavity, as well as on immune and other oral immune-supporting cells and their role in oral inflammatory responses.

Prof. Dr. Peter Proff
Guest Editor

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

Oral inflammation
Oral immunology
Oral malformations
Periodontitis
Environment signals
Cellular signaling
Imaging

Related Special Issue

Oral Inflammation—Environment, Molecules, and Cells in Oral Physiology and Pathology in International Journal of Molecular Sciences (22 articles)

Published Papers (14 papers)

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Jump to: Review

20 pages, 30708 KiB

Open AccessArticle

Zoledronate Causes a Systemic Shift of Macrophage Polarization towards M1 In Vivo

by Manuel Weber, Andi Homm, Stefan Müller, Silke Frey, Kerstin Amann, Jutta Ries, Carol Geppert, Raimund Preidl, Tobias Möst, Peer W. Kämmerer, Marco Kesting and Falk Wehrhan

Int. J. Mol. Sci. 2021, 22(3), 1323; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22031323 - 28 Jan 2021

Cited by 16 | Viewed by 2842

Abstract

Background: Immunomodulatory properties of bisphosphonates (BP) are suggested to contribute to the development of medication-associated osteonecrosis of the jaw (MRONJ). Furthermore, bisphosphonate-derived immune modulation might contribute to the anti-metastatic effect observed in breast cancer patients. Macrophages are potential candidates for the mediation of immunomodulatory effects of bisphosphonates. The study aimed to investigate the influence of bisphosphonates alone and in combination with surgical trauma on systemic macrophage polarization (M1 vs. M2) using an in vivo rat model. Methods: A total of 120 animals were divided into four groups. Groups 2 and 4 were treated with 8 × 40 μg/kg body weight of the BP Zoledronate i.p. (week 0–7). Groups 3 and 4 were exposed to surgical trauma (week 8, tooth extraction + tibia fracture), whereas in Group 1 neither medication nor surgical trauma was applied. After 8, 10, 12 and 16 weeks, skin, lung and spleen were immunohistochemically examined for macrophage polarization via expression analysis of CD68, CD163 and iNOS using a tissue microarray (TMA). Results: A significant shift of macrophage polarization towards M1 was observed in skin, spleen and lung tissue of animals, with and without surgical trauma, treated with BP when compared to those without BP application. Surgical trauma did not cause a significant increase towards M1 polarization. Conclusions: BP application leads to a systemic pro-inflammatory situation in vivo, independent of surgical trauma, as evidenced by the shift in macrophage polarization towards M1 in various somatic tissues. This provides a possible explanation for the clinically observed anti-tumor effect of bisphosphonates and might also contribute to pathogenesis of MRONJ. Full article

(This article belongs to the Special Issue Oral Inflammation—Environment, Molecules, and Cells in Oral Physiology and Pathology)

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16 pages, 12851 KiB

Open AccessArticle

Filifactor alocis and Tumor Necrosis Factor-Alpha Stimulate Synthesis of Visfatin by Human Macrophages

by Andressa Vilas Boas Nogueira, Marjan Nokhbehsaim, Anna Damanaki, Sigrun Eick, Christian Kirschneck, Agnes Schröder, Jonathan Jantsch and James Deschner

Int. J. Mol. Sci. 2021, 22(3), 1235; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22031235 - 27 Jan 2021

Cited by 11 | Viewed by 1999

Abstract

There is little known about the effect of the periodontopathogen Filifactor alocis on macrophages as key cells of the innate immune defense in the periodontium. Therefore, the aim of the present study was to investigate the effect of F. alocis and additionally of the pro-inflammatory cytokine tumor necrosis factor-alpha (TNFα) on visfatin and other pro-inflammatory and proteolytic molecules associated with periodontitis in human macrophages. The presence of macrophage markers CD14, CD86, CD68, and CD163 was examined in gingival biopsies from healthy individuals and periodontitis patients. Human macrophages were incubated with F. alocis and TNFα for up to 2 d. The effects of both stimulants on macrophages were determined by real-time PCR, ELISA, immunocytochemistry, and immunofluorescence. F. alocis was able to significantly stimulate the synthesis of visfatin by human macrophages using TLR2 and MAPK pathways. In addition to visfatin, F. alocis was also able to increase the synthesis of cyclooxygenase 2, TNFα, and matrix metalloproteinase 1. Like F. alocis, TNFα was also able to stimulate the production of these proinflammatory and proteolytic molecules. Our results highlight the pathogenetic role of F. alocis in periodontal diseases and also underline the involvement of visfatin in the aetiopathogenesis of periodontitis. Full article

(This article belongs to the Special Issue Oral Inflammation—Environment, Molecules, and Cells in Oral Physiology and Pathology)

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14 pages, 2779 KiB

Open AccessArticle

Dietary Salt Accelerates Orthodontic Tooth Movement by Increased Osteoclast Activity

by Agnes Schröder, Joshua Gubernator, Alexandra Leikam, Ute Nazet, Fabian Cieplik, Jonathan Jantsch, Patrick Neubert, Jens Titze, Peter Proff and Christian Kirschneck

Int. J. Mol. Sci. 2021, 22(2), 596; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22020596 - 09 Jan 2021

Cited by 4 | Viewed by 2413

Abstract

Dietary salt uptake and inflammation promote sodium accumulation in tissues, thereby modulating cells like macrophages and fibroblasts. Previous studies showed salt effects on periodontal ligament fibroblasts and on bone metabolism by expression of nuclear factor of activated T-cells-5 (NFAT-5). Here, we investigated the impact of salt and NFAT-5 on osteoclast activity and orthodontic tooth movement (OTM). After treatment of osteoclasts without (NS) or with additional salt (HS), we analyzed gene expression and the release of tartrate-resistant acid phosphatase and calcium phosphate resorption. We kept wild-type mice and mice lacking NFAT-5 in myeloid cells either on a low, normal or high salt diet and inserted an elastic band between the first and second molar to induce OTM. We analyzed the expression of genes involved in bone metabolism, periodontal bone loss, OTM and bone density. Osteoclast activity was increased upon HS treatment. HS promoted periodontal bone loss and OTM and was associated with reduced bone density. Deletion of NFAT-5 led to increased osteoclast activity with NS, whereas we detected impaired OTM in mice. Dietary salt uptake seems to accelerate OTM and induce periodontal bone loss due to reduced bone density, which may be attributed to enhanced osteoclast activity. NFAT-5 influences this reaction to HS, as we detected impaired OTM and osteoclast activity upon deletion. Full article

(This article belongs to the Special Issue Oral Inflammation—Environment, Molecules, and Cells in Oral Physiology and Pathology)

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16 pages, 2416 KiB

Open AccessArticle

Regulation of Anti-Apoptotic SOD2 and BIRC3 in Periodontal Cells and Tissues

by Birgit Rath-Deschner, Andressa Vilas Boas Nogueira, Svenja Memmert, Marjan Nokhbehsaim, Joni Augusto Cirelli, Sigrun Eick, Nicolai Miosge, Christian Kirschneck, Marco Kesting, James Deschner, Andreas Jäger and Anna Damanaki

Int. J. Mol. Sci. 2021, 22(2), 591; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22020591 - 08 Jan 2021

Cited by 11 | Viewed by 2039

Abstract

The aim of the study was to clarify whether orthodontic forces and periodontitis interact with respect to the anti-apoptotic molecules superoxide dismutase 2 (SOD2) and baculoviral IAP repeat-containing protein 3 (BIRC3). SOD2, BIRC3, and the apoptotic markers caspases 3 (CASP3) and 9 (CASP9) were analyzed in gingiva from periodontally healthy and periodontitis subjects by real-time PCR and immunohistochemistry. SOD2 and BIRC3 were also studied in gingiva from rats with experimental periodontitis and/or orthodontic tooth movement. Additionally, SOD2 and BIRC3 levels were examined in human periodontal fibroblasts incubated with Fusobacterium nucleatum and/or subjected to mechanical forces. Gingiva from periodontitis patients showed significantly higher SOD2, BIRC3, CASP3, and CASP9 levels than periodontally healthy gingiva. SOD2 and BIRC3 expressions were also significantly increased in the gingiva from rats with experimental periodontitis, but the upregulation of both molecules was significantly diminished in the concomitant presence of orthodontic tooth movement. In vitro, SOD2 and BIRC3 levels were significantly increased by F. nucleatum, but this stimulatory effect was also significantly inhibited by mechanical forces. Our study suggests that SOD2 and BIRC3 are produced in periodontal infection as a protective mechanism against exaggerated apoptosis. In the concomitant presence of orthodontic forces, this protective anti-apoptotic mechanism may get lost. Full article

(This article belongs to the Special Issue Oral Inflammation—Environment, Molecules, and Cells in Oral Physiology and Pathology)

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13 pages, 6949 KiB

Open AccessArticle

Inflammation in the Human Periodontium Induces Downregulation of the α₁- and β₁-Subunits of the sGC in Cementoclasts

by Yüksel Korkmaz, Behrus Puladi, Kerstin Galler, Peer W. Kämmerer, Agnes Schröder, Lina Gölz, Tim Sparwasser, Wilhelm Bloch, Andreas Friebe and James Deschner

Int. J. Mol. Sci. 2021, 22(2), 539; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22020539 - 07 Jan 2021

Cited by 4 | Viewed by 2820

Abstract

Nitric oxide (NO) binds to soluble guanylyl cyclase (sGC), activates it in a reduced oxidized heme iron state, and generates cyclic Guanosine Monophosphate (cGMP), which results in vasodilatation and inhibition of osteoclast activity. In inflammation, sGC is oxidized and becomes insensitive to NO. NO- and heme-independent activation of sGC requires protein expression of the α₁- and β₁-subunits. Inflammation of the periodontium induces the resorption of cementum by cementoclasts and the resorption of the alveolar bone by osteoclasts, which can lead to tooth loss. As the presence of sGC in cementoclasts is unknown, we investigated the α₁- and β₁-subunits of sGC in cementoclasts of healthy and inflamed human periodontium using double immunostaining for CD68 and cathepsin K and compared the findings with those of osteoclasts from the same sections. In comparison to cementoclasts in the healthy periodontium, cementoclasts under inflammatory conditions showed a decreased staining intensity for both α₁- and β₁-subunits of sGC, indicating reduced protein expression of these subunits. Therefore, pharmacological activation of sGC in inflamed periodontal tissues in an NO- and heme-independent manner could be considered as a new treatment strategy to inhibit cementum resorption. Full article

(This article belongs to the Special Issue Oral Inflammation—Environment, Molecules, and Cells in Oral Physiology and Pathology)

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16 pages, 2067 KiB

Open AccessArticle

Role and Regulation of Mechanotransductive HIF-1α Stabilisation in Periodontal Ligament Fibroblasts

by Christian Kirschneck, Magdalena Thuy, Alexandra Leikam, Svenja Memmert, James Deschner, Anna Damanaki, Gerrit Spanier, Peter Proff, Jonathan Jantsch and Agnes Schröder

Int. J. Mol. Sci. 2020, 21(24), 9530; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21249530 - 15 Dec 2020

Cited by 8 | Viewed by 2293

Abstract

Orthodontic tooth movement (OTM) creates compressive and tensile strain in the periodontal ligament, causing circulation disorders. Hypoxia-inducible factor 1α (HIF-1α) has been shown to be primarily stabilised by compression, but not hypoxia in periodontal ligament fibroblasts (PDLF) during mechanical strain, which are key regulators of OTM. This study aimed to elucidate the role of heparan sulfate integrin interaction and downstream kinase phosphorylation for HIF-1α stabilisation under compressive and tensile strain and to which extent downstream synthesis of VEGF and prostaglandins is HIF-1α-dependent in a model of simulated OTM in PDLF. PDLF were subjected to compressive or tensile strain for 48 h. In various setups HIF-1α was experimentally stabilised (DMOG) or destabilised (YC-1) and mechanotransduction was inhibited by surfen and genistein. We found that HIF-1α was not stabilised by tensile, but rather by compressive strain. HIF-1α stabilisation had an inductive effect on prostaglandin and VEGF synthesis. As expected, HIF-1α destabilisation reduced VEGF expression, whereas prostaglandin synthesis was increased. Inhibition of integrin mechanotransduction via surfen or genistein prevented stabilisation of HIF-1α. A decrease in VEGF expression was observed, but not in prostaglandin synthesis. Stabilisation of HIF-1α via integrin mechanotransduction and downstream phosphorylation of kinases seems to be essential for the induction of VEGF, but not prostaglandin synthesis by PDLF during compressive (but not tensile) orthodontic strain. Full article

(This article belongs to the Special Issue Oral Inflammation—Environment, Molecules, and Cells in Oral Physiology and Pathology)

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15 pages, 882 KiB

Open AccessArticle

Regulation of Autophagic Signaling by Mechanical Loading and Inflammation in Human PDL Fibroblasts

by Kim Blawat, Alexandra Mayr, Miriam Hardt, Christian Kirschneck, Marjan Nokhbehsaim, Christian Behl, James Deschner, Andreas Jäger and Svenja Memmert

Int. J. Mol. Sci. 2020, 21(24), 9446; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21249446 - 11 Dec 2020

Cited by 13 | Viewed by 1833

Abstract

Autophagy (cellular self-consumption) is a crucial adaptation mechanism during cellular stress conditions. This study aimed to examine how this important process is regulated in human periodontal ligament (PDL) fibroblasts by mechanical and inflammatory stress conditions and whether the mammalian target of rapamycin (mTOR) signaling pathway is involved. Autophagy was quantified by flow cytometry. Qualitative protein phosphorylation profiling of the mTOR pathway was carried out. Effects of mTOR regulation were assessed by quantification of important synthesis product collagen 1, cell proliferation and cell death with real-time PCR and flow cytometry. Autophagy as a response to mechanical or inflammatory treatment in PDL fibroblasts was dose and time dependent. In general, autophagy was induced by stress stimulation. Phosphorylation analysis of mTOR showed regulatory influences of mechanical and inflammatory stimulation on crucial target proteins. Regulation of mTOR was also detectable via changes in protein synthesis and cell proliferation. Physiological pressure had cell-protective effects (p = 0.025), whereas overload increased cell death (p = 0.003), which was also promoted in long-term inflammatory treatment (p < 0.001). Our data provide novel insights about autophagy regulation by mechanical and inflammatory stress conditions in human PDL fibroblasts. Our results suggest some involvement of the mTOR pathway in autophagy and cell fate regulation under the named conditions. Full article

(This article belongs to the Special Issue Oral Inflammation—Environment, Molecules, and Cells in Oral Physiology and Pathology)

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22 pages, 3206 KiB

Open AccessArticle

Defining Metaniches in the Oral Cavity According to Their Microbial Composition and Cytokine Profile

by Corinna L. Seidel, Roman G. Gerlach, Patrick Wiedemann, Matthias Weider, Gabriele Rodrian, Michael Hader, Benjamin Frey, Udo S. Gaipl, Aline Bozec, Fabian Cieplik, Christian Kirschneck, Christian Bogdan and Lina Gölz

Int. J. Mol. Sci. 2020, 21(21), 8218; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21218218 - 03 Nov 2020

Cited by 16 | Viewed by 2654

Abstract

The human oral microbiota consists of over 700 widespread taxa colonizing the oral cavity in several anatomically diverse oral niches. Lately, sequencing of the 16S rRNA genes has become an acknowledged, culture-independent method to characterize the oral microbiota. However, only a small amount of data are available concerning microbial differences between oral niches in periodontal health and disease. In the context of periodontitis, the cytokine expression in the gingival crevicular fluid has been studied in detail, whereas little is known about the cytokine profile in hard and soft tissue biofilms. In order to characterize oral niches in periodontal health, the oral microbiota and cytokine pattern were analyzed at seven different sites (plaque (P), gingival crevicular fluid (GCF), saliva (S), tongue (T), hard palate (HP), cheek (C) and sublingual area (U)) of 20 young adults using next-generation sequencing and multiplex immunoassays. Site-specific microbial compositions were detected, which clustered into three distinct metaniches (“P-GCF”, “S-T-HP” and “C-U”) and were associated with niche-/metaniche-specific cytokine profiles. Our findings allow the definition of distinct metaniches according to their microbial composition, partly reflected by their cytokine profile, and provide new insights into microenvironmental similarities between anatomical diverse oral niches. Full article

(This article belongs to the Special Issue Oral Inflammation—Environment, Molecules, and Cells in Oral Physiology and Pathology)

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10 pages, 1711 KiB

Open AccessArticle

A Human Periodontal Ligament Fibroblast Cell Line as a New Model to Study Periodontal Stress

by Matthias Weider, Agnes Schröder, Denitsa Docheva, Gabriele Rodrian, Isabel Enderle, Corinna Lesley Seidel, Darja Andreev, Michael Wegner, Aline Bozec, James Deschner, Christian Kirschneck, Peter Proff and Lina Gölz

Int. J. Mol. Sci. 2020, 21(21), 7961; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21217961 - 27 Oct 2020

Cited by 12 | Viewed by 2553

Abstract

The periodontal ligament (PDL) is exposed to different kinds of mechanical stresses such as bite force or orthodontic tooth movement. A simple and efficient model to study molecular responses to mechanical stress is the application of compressive force onto primary human periodontal ligament fibroblasts via glass disks. Yet, this model suffers from the need for primary cells from human donors which have a limited proliferative capacity. Here we show that an immortalized cell line, PDL-hTERT, derived from primary human periodontal ligament fibroblasts exhibits characteristic responses to glass disk-mediated compressive force resembling those of primary cells. These responses include induction and secretion of pro-inflammatory markers, changes in expression of extracellular matrix-reorganizing genes and induction of genes related to angiogenesis, osteoblastogenesis and osteoclastogenesis. The fact that PDL-hTERT cells can easily be transfected broadens their usefulness, as molecular gain- and loss-of-function studies become feasible. Full article

(This article belongs to the Special Issue Oral Inflammation—Environment, Molecules, and Cells in Oral Physiology and Pathology)

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26 pages, 10163 KiB

Open AccessArticle

In Vivo Modulation of Angiogenesis and Immune Response on a Collagen Matrix via Extracorporeal Shockwaves

by Diana Heimes, Nadine Wiesmann, Jonas Eckrich, Juergen Brieger, Stefan Mattyasovszky, Peter Proff, Manuel Weber, James Deschner, Bilal Al-Nawas and Peer W. Kämmerer

Int. J. Mol. Sci. 2020, 21(20), 7574; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21207574 - 14 Oct 2020

Cited by 20 | Viewed by 2849

Abstract

The effective management of tissue integration and immunological responses to transplants decisively co-determines the success of soft and hard tissue reconstruction. The aim of this in vivo study was to evaluate the eligibility of extracorporeal shock wave therapy (ESWT) with respect to its ability to modulate angiogenesis and immune response to a collagen matrix (CM) for tissue engineering in the chorioallantoic membrane (CAM) assay, which is performed with fertilized chicken eggs. CM were placed on the CAM on embryonic development day (EDD) 7; at EDD-10, ESWT was conducted at 0.12 mJ/mm² with 500 impulses each. One and four days later, angiogenesis represented by vascularized area, vessel density, and vessel junctions as well as HIF-1α and VEGF gene expression were evaluated. Furthermore, immune response (iNOS2, MMP-9, and MMP-13 via qPCR) was assessed and compared between ESWT- and non-ESWT-groups. At EDD-14, the vascularized area (+115% vs. +26%) and the increase in vessel junctions (+751% vs. +363%) were significantly higher in the ESWT-group. ESWT significantly increased MMP-9 gene expression at EDD-11 and significantly decreased MMP-13 gene expression at EDD-14 as compared to the controls. Using the CAM assay, an enhanced angiogenesis and neovascularization in CM after ESWT were observed. Furthermore, ESWT could reduce the inflammatory activity after a latency of four days. Full article

(This article belongs to the Special Issue Oral Inflammation—Environment, Molecules, and Cells in Oral Physiology and Pathology)

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21 pages, 10870 KiB

Open AccessReview

Is Inflammation a Friend or Foe for Orthodontic Treatment?: Inflammation in Orthodontically Induced Inflammatory Root Resorption and Accelerating Tooth Movement

by Masaru Yamaguchi and Shinichi Fukasawa

Int. J. Mol. Sci. 2021, 22(5), 2388; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22052388 - 27 Feb 2021

Cited by 65 | Viewed by 9286

Abstract

The aim of this paper is to provide a review on the role of inflammation in orthodontically induced inflammatory root resorption (OIIRR) and accelerating orthodontic tooth movement (AOTM) in orthodontic treatment. Orthodontic tooth movement (OTM) is stimulated by remodeling of the periodontal ligament (PDL) and alveolar bone. These remodeling activities and tooth displacement are involved in the occurrence of an inflammatory process in the periodontium, in response to orthodontic forces. Inflammatory mediators such as prostaglandins (PGs), interleukins (Ils; IL-1, -6, -17), the tumor necrosis factor (TNF)-α superfamily, and receptor activator of nuclear factor (RANK)/RANK ligand (RANKL)/osteoprotegerin (OPG) are increased in the PDL during OTM. OIIRR is one of the accidental symptoms, and inflammatory mediators have been detected in resorbed roots, PDL, and alveolar bone exposed to heavy orthodontic force. Therefore, these inflammatory mediators are involved with the occurrence of OIIRR during orthodontic tooth movement. On the contrary, regional accelerating phenomenon (RAP) occurs after fractures and surgery such as osteotomies or bone grafting, and bone healing is accelerated by increasing osteoclasts and osteoblasts. Recently, tooth movement after surgical procedures such as corticotomy, corticision, piezocision, and micro-osteoperforation might be accelerated by RAP, which increases the bone metabolism. Therefore, inflammation may be involved in accelerated OTM (AOTM). The knowledge of inflammation during orthodontic treatment could be used in preventing OIIRR and AOTM. Full article

(This article belongs to the Special Issue Oral Inflammation—Environment, Molecules, and Cells in Oral Physiology and Pathology)

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23 pages, 2310 KiB

Open AccessReview

Inflammatory Response Mechanisms of the Dentine–Pulp Complex and the Periapical Tissues

by Kerstin M. Galler, Manuel Weber, Yüksel Korkmaz, Matthias Widbiller and Markus Feuerer

Int. J. Mol. Sci. 2021, 22(3), 1480; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22031480 - 02 Feb 2021

Cited by 133 | Viewed by 15904

Abstract

The macroscopic and microscopic anatomy of the oral cavity is complex and unique in the human body. Soft-tissue structures are in close interaction with mineralized bone, but also dentine, cementum and enamel of our teeth. These are exposed to intense mechanical and chemical stress as well as to dense microbiologic colonization. Teeth are susceptible to damage, most commonly to caries, where microorganisms from the oral cavity degrade the mineralized tissues of enamel and dentine and invade the soft connective tissue at the core, the dental pulp. However, the pulp is well-equipped to sense and fend off bacteria and their products and mounts various and intricate defense mechanisms. The front rank is formed by a layer of odontoblasts, which line the pulp chamber towards the dentine. These highly specialized cells not only form mineralized tissue but exert important functions as barrier cells. They recognize pathogens early in the process, secrete antibacterial compounds and neutralize bacterial toxins, initiate the immune response and alert other key players of the host defense. As bacteria get closer to the pulp, additional cell types of the pulp, including fibroblasts, stem and immune cells, but also vascular and neuronal networks, contribute with a variety of distinct defense mechanisms, and inflammatory response mechanisms are critical for tissue homeostasis. Still, without therapeutic intervention, a deep carious lesion may lead to tissue necrosis, which allows bacteria to populate the root canal system and invade the periradicular bone via the apical foramen at the root tip. The periodontal tissues and alveolar bone react to the insult with an inflammatory response, most commonly by the formation of an apical granuloma. Healing can occur after pathogen removal, which is achieved by disinfection and obturation of the pulp space by root canal treatment. This review highlights the various mechanisms of pathogen recognition and defense of dental pulp cells and periradicular tissues, explains the different cell types involved in the immune response and discusses the mechanisms of healing and repair, pointing out the close links between inflammation and regeneration as well as between inflammation and potential malignant transformation. Full article

(This article belongs to the Special Issue Oral Inflammation—Environment, Molecules, and Cells in Oral Physiology and Pathology)

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15 pages, 1004 KiB

Open AccessReview

The Special Developmental Biology of Craniofacial Tissues Enables the Understanding of Oral and Maxillofacial Physiology and Diseases

by Manuel Weber, Falk Wehrhan, James Deschner, Janina Sander, Jutta Ries, Tobias Möst, Aline Bozec, Lina Gölz, Marco Kesting and Rainer Lutz

Int. J. Mol. Sci. 2021, 22(3), 1315; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22031315 - 28 Jan 2021

Cited by 5 | Viewed by 2973

Abstract

Maxillofacial hard tissues have several differences compared to bones of other localizations of the human body. These could be due to the different embryological development of the jaw bones compared to the extracranial skeleton. In particular, the immigration of neuroectodermally differentiated cells of the cranial neural crest (CNC) plays an important role. These cells differ from the mesenchymal structures of the extracranial skeleton. In the ontogenesis of the jaw bones, the development via the intermediate stage of the pharyngeal arches is another special developmental feature. The aim of this review was to illustrate how the development of maxillofacial hard tissues occurs via the cranial neural crest and pharyngeal arches, and what significance this could have for relevant pathologies in maxillofacial surgery, dentistry and orthodontic therapy. The pathogenesis of various growth anomalies and certain syndromes will also be discussed. Full article

(This article belongs to the Special Issue Oral Inflammation—Environment, Molecules, and Cells in Oral Physiology and Pathology)

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19 pages, 2301 KiB

Open AccessReview

Influence of Natural Killer Cells and Natural Killer T Cells on Periodontal Disease: A Systematic Review of the Current Literature

by Andreas Seidel, Corinna L. Seidel, Matthias Weider, Rüdiger Junker, Lina Gölz and Helga Schmetzer

Int. J. Mol. Sci. 2020, 21(24), 9766; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21249766 - 21 Dec 2020

Cited by 11 | Viewed by 3138

Abstract

Natural killer (NK) cells, as members of the innate immune system, and natural killer T (NKT) cells, bridging innate and adaptive immunity, play a prominent role in chronic inflammatory diseases and cancerogenesis, yet have scarcely been examined in oral diseases. Therefore, systematic research on the latest literature focusing on NK/NKT cell-mediated mechanisms in periodontal disease, including the time period 1988–2020, was carried out in MEDLINE (PubMed) using a predetermined search strategy, with a final selection of 25 studies. The results showed that NK cells tend to have rather proinflammatory influences via cytokine production, cytotoxic effects, dendritic-cell-crosstalk, and autoimmune reactions, while contrarily, NKT cell-mediated mechanisms were proinflammatory and immunoregulatory, ranging from protective effects via B-cell-regulation, specific antibody production, and the suppression of autoimmunity to destructive effects via cytokine production, dendritic-cell-crosstalk, and T-/B-cell interactions. Since NK cells seem to have a proinflammatory role in periodontitis, further research should focus on the proinflammatory and immunoregulatory properties of NKT cells in order to create, in addition to antibacterial strategies in dental inflammatory disease, novel anti-inflammatory therapeutic approaches modulating host immunity towards dental health. Full article

(This article belongs to the Special Issue Oral Inflammation—Environment, Molecules, and Cells in Oral Physiology and Pathology)

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