Submit to IJMS Review for IJMS Propose a Special Issue

Journal Menu

Journal Browser

Molecular Mechanisms of Periodontal Disease 2.0

Print Special Issue Flyer
Special Issue Editors
Special Issue Information
Keywords
Related Special Issues
Published Papers

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 January 2022) | Viewed by 40540

Share This Special Issue

Special Issue Editor

Prof. Dr. Mikihito Kajiya

E-Mail Website
Guest Editor

Department of Periodontal Medicine, Applied Life Sciences, Institute of Biomedical & Health Sciences, Graduate School of Biomedical & Health Sciences, Hiroshima University, Minami-ku, Hiroshima, Japan
Interests: stem cells; bone biology; signal transduction; cytokines
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Periodontitis is a chronic inflammatory disease characterized by lymphocytic infiltration and alveolar bone destruction, along with tooth loss. Accumulated lines of evidence suggest that such destructive inflammation is elicited by host innate and adaptive immune response to periodontal biofilm-associated multiple microorganisms. In addition, several inflammatory cytokines produced from lymphocytes, leukocytes, fibroblasts, and gingival epithelial cells in the context of host immune responses have been identified as key molecules inducing periodontal tissue destruction. More specifically, proinflammatory cytokines, including IL-6 and IL-17, facilitate the RNAKL expression level in fibroblasts or lymphocytes, which results in the induction of bone resorption. However, despite advances in our understanding of its etiology, scientific endeavors to fight against periodontal disease have progressed little. Accordingly, it is required to deepen our understanding of a more detailed molecular mechanism of the immune system against oral microorganisms to develop preventive or therapeutic regimens. To that end, this Special Issue, which is a continuation of a previous successful issue on the molecular mechanisms of periodontal disease, focuses on novel immune reaction systems from the molecular level (microbe, microRNA, inflammatory cytokine signaling cascade, etc.) to the cellular level (Th1, Th2, Th17, Treg, and B cells activity, osteoclastogenesis, dendritic cells and monocytes immune response, the role of fibroblasts/epithelial cells in inflammation, etc.) in mouse periodontal disease models.

Thanks to everyone, our first special issue, “Molecular Mechanism of Periodontal Disease,” was a huge success. Hopefully, we can proceed with understanding periodontal disease to the higher stage with the relaunched special issue.

Prof. Dr. Mikihito Kajiya
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

periodontitis
immune response
periodontal pathogens
bone resorption
RANKL

Related Special Issues

Molecular Mechanisms of Periodontal Disease in International Journal of Molecular Sciences (23 articles)
Molecular Mechanisms of Periodontal Disease 3.0 in International Journal of Molecular Sciences (5 articles)

Published Papers (11 papers)

Download All Papers

Research

Jump to: Review

18 pages, 3535 KiB

Open AccessArticle

Locally Secreted Semaphorin 4D Is Engaged in Both Pathogenic Bone Resorption and Retarded Bone Regeneration in a Ligature-Induced Mouse Model of Periodontitis

by Takenobu Ishii, Montserrat Ruiz-Torruella, Kenta Yamamoto, Tsuguno Yamaguchi, Alireza Heidari, Roodelyne Pierrelus, Elizabeth Leon, Satoru Shindo, Mohamad Rawas-Qalaji, Maria Rita Pastore, Atsushi Ikeda, Shin Nakamura, Hani Mawardi, Umadevi Kandalam, Patrick Hardigan, Lukasz Witek, Paulo G. Coelho and Toshihisa Kawai

Int. J. Mol. Sci. 2022, 23(10), 5630; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23105630 - 18 May 2022

Cited by 7 | Viewed by 2756

Abstract

It is well known that Semaphorin 4D (Sema4D) inhibits IGF-1-mediated osteogenesis by binding with PlexinB1 expressed on osteoblasts. However, its elevated level in the gingival crevice fluid of periodontitis patients and the broader scope of its activities in the context of potential upregulation of osteoclast-mediated periodontal bone-resorption suggest the need for further investigation of this multifaceted molecule. In short, the pathophysiological role of Sema4D in periodontitis requires further study. Accordingly, attachment of the ligature to the maxillary molar of mice for 7 days induced alveolar bone-resorption accompanied by locally elevated, soluble Sema4D (sSema4D), TNF-α and RANKL. Removal of the ligature induced spontaneous bone regeneration during the following 14 days, which was significantly promoted by anti-Sema4D-mAb administration. Anti-Sema4D-mAb was also suppressed in vitro osteoclastogenesis and pit formation by RANKL-stimulated BMMCs. While anti-Sema4D-mAb downmodulated the bone-resorption induced in mouse periodontitis, it neither affected local production of TNF-α and RANKL nor systemic skeletal bone remodeling. RANKL-induced osteoclastogenesis and resorptive activity were also suppressed by blocking of CD72, but not Plexin B2, suggesting that sSema4D released by osteoclasts promotes osteoclastogenesis via ligation to CD72 receptor. Overall, our data indicated that ssSema4D released by osteoclasts may play a dual function by decreasing bone formation, while upregulating bone-resorption. Full article

(This article belongs to the Special Issue Molecular Mechanisms of Periodontal Disease 2.0)

► Show Figures

Figure 1

14 pages, 2187 KiB

Open AccessArticle

Dual-Function Semaphorin 4D Released by Platelets: Suppression of Osteoblastogenesis and Promotion of Osteoclastogenesis

by Satoru Shindo, Irma Josefina Savitri, Takenobu Ishii, Atsushi Ikeda, Roodelyne Pierrelus, Alireza Heidari, Keisuke Okubo, Shin Nakamura, Umadevi Kandalam, Mohamad Rawas-Qalaji, Elizabeth Leon, Maria Rita Pastore, Patrick Hardigan and Toshihisa Kawai

Int. J. Mol. Sci. 2022, 23(6), 2938; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23062938 - 09 Mar 2022

Cited by 9 | Viewed by 2192

Abstract

Effects of the antiosteoblastogenesis factor Semaphorin 4D (Sema4D), expressed by thrombin-activated platelets (TPs), on osteoblastogenesis, as well as osteoclastogenesis, were investigated in vitro. Intact platelets released both Sema4D and IGF-1. However, in response to stimulation with thrombin, platelets upregulated the release of Sema4D, but not IGF-1. Anti-Sema4D-neutralizing monoclonal antibody (mAb) upregulated TP-mediated osteoblastogenesis in MC3T3-E1 osteoblast precursors. MC3T3-E1 cells exposed to TPs induced phosphorylation of Akt and ERK further upregulated by the addition of anti-sema4D-mAb, suggesting the suppressive effects of TP-expressing Sema4D on osteoblastogenesis. On the other hand, TPs promoted RANKL-mediated osteoclastogenesis in the primary culture of bone-marrow-derived mononuclear cells (BMMCs). Among the known three receptors of Sema4D, including Plexin B1, Plexin B2 and CD72, little Plexin B2 was detected, and no Plexin B1 was detected, but a high level of CD72 mRNA was detected in RANKL-stimulated BMMCs by qPCR. Both anti-Sema4D-mAb and anti-CD72-mAb suppressed RANKL-induced osteoclast formation and bone resorptive activity, suggesting that Sema4D released by TPs promotes osteoclastogenesis via ligation to a CD72 receptor. This study demonstrated that Sema4D released by TPs suppresses osteogenic activity and promotes osteoclastogenesis, suggesting the novel property of platelets in bone-remodeling processes. Full article

(This article belongs to the Special Issue Molecular Mechanisms of Periodontal Disease 2.0)

► Show Figures

Figure 1

13 pages, 1733 KiB

Open AccessArticle

GDF15 Supports the Inflammatory Response of PdL Fibroblasts Stimulated by P. gingivalis LPS and Concurrent Compression

by Albert Stemmler, Judit Symmank, Julia Steinmetz, Katrin von Brandenstein, Christoph-Ludwig Hennig and Collin Jacobs

Int. J. Mol. Sci. 2021, 22(24), 13608; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms222413608 - 19 Dec 2021

Cited by 9 | Viewed by 2751

Abstract

Periodontitis is characterized by bacterially induced inflammatory destruction of periodontal tissue. This also affects fibroblasts of the human periodontal ligaments (HPdLF), which play a coordinating role in force-induced tissue and alveolar bone remodeling. Excessive inflammation in the oral tissues has been observed with simultaneous stimulation by pathogens and mechanical forces. Recently, elevated levels of growth differentiation factor 15 (GDF15), an immuno-modulatory member of the transforming growth factor (TGFB) superfamily, were detected under periodontitis-like conditions and in force-stressed PdL cells. In view of the pleiotropic effects of GDF15 in various tissues, this study aims to investigate the role of GDF15 in P. gingivalis-related inflammation of HPdLF and its effect on the excessive inflammatory response to concurrent compressive stress. To this end, the expression and secretion of cytokines (IL6, IL8, COX2/PGE2, TNFα) and the activation of THP1 monocytic cells were analyzed in GDF15 siRNA-treated HPdLF stimulated with P. gingivalis lipopolysaccharides alone and in combination with compressive force. GDF15 knockdown significantly reduced cytokine levels and THP1 activation in LPS-stimulated HPdLF, which was less pronounced with additional compressive stress. Overall, our data suggest a pro-inflammatory role for GDF15 in periodontal disease and demonstrate that GDF15 partially modulates the force-induced excessive inflammatory response of PdLF under these conditions. Full article

(This article belongs to the Special Issue Molecular Mechanisms of Periodontal Disease 2.0)

► Show Figures

Figure 1

16 pages, 2609 KiB

Open AccessArticle

The Selective Histone Deacetylase Inhibitor MI192 Enhances the Osteogenic Differentiation Efficacy of Human Dental Pulp Stromal Cells

by Kenny Man, Liam Lawlor, Lin-Hua Jiang and Xuebin B. Yang

Int. J. Mol. Sci. 2021, 22(10), 5224; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22105224 - 14 May 2021

Cited by 17 | Viewed by 2406

Abstract

The use of human dental pulp stromal cells (hDPSCs) has gained increasing attention as an alternative stem cell source for bone tissue engineering. The modification of the cells’ epigenetics has been found to play an important role in regulating differentiation, with the inhibition of histone deacetylases 3 (HDAC3) being linked to increased osteogenic differentiation. This study aimed to induce epigenetic reprogramming using the HDAC2 and 3 selective inhibitor, MI192 to promote hDPSCs osteogenic capacity for bone regeneration. MI192 treatment caused a time–dose-dependent change in hDPSC morphology and reduction in viability. Additionally, MI192 successfully augmented hDPSC epigenetic functionality, which resulted in increased histone acetylation and cell cycle arrest at the G₂/M phase. MI192 pre-treatment exhibited a dose-dependent effect on hDPSCs alkaline phosphatase activity. Quantitative PCR and In-Cell Western further demonstrated that MI192 pre-treatment significantly upregulated hDPSCs osteoblast-related gene and protein expression (alkaline phosphatase, bone morphogenic protein 2, type I collagen and osteocalcin) during osteogenic differentiation. Importantly, MI192 pre-treatment significantly increased hDPSCs extracellular matrix collagen production and mineralisation. As such, for the first time, our findings show that epigenetic reprogramming with the HDAC2 and 3 selective inhibitor MI192 accelerates the osteogenic differentiation of hDPSCs, demonstrating the considerable utility of this MSCs engineering approach for bone augmentation strategies. Full article

(This article belongs to the Special Issue Molecular Mechanisms of Periodontal Disease 2.0)

► Show Figures

Graphical abstract

12 pages, 7750 KiB

Open AccessArticle

AT1 and AT2 Receptor Knockout Changed Osteonectin and Bone Density in Mice in Periodontal Inflammation Experimental Model

by Maria Laura de Souza Lima, Caroline Addison Carvalho Xavier de Medeiros, Gerlane Coelho Bernardo Guerra, Robson Santos, Michael Bader, Flavia Q. Pirih, Raimundo Fernandes de Araújo Júnior, Alan B. Chan, Luis J. Cruz, Gerly Anne de Castro Brito, Renata Ferreira de Carvalho Leitão, Ericka Janine Dantas da Silveira, Vinicius Barreto Garcia, Agnes Andrade Martins and Aurigena Antunes de Araújo

Int. J. Mol. Sci. 2021, 22(10), 5217; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22105217 - 14 May 2021

Cited by 4 | Viewed by 2415

Abstract

Background: The aim of this study was to evaluate the role of AT1 and AT2 receptors in a periodontal inflammation experimental model. Methods: Periodontal inflammation was induced by LPS/Porphyromonas gingivalis. Maxillae, femur, and vertebra were scanned using Micro-CT. Maxillae were analyzed histopathologically, immunohistochemically, and by RT-PCR. Results: The vertebra showed decreased BMD in AT1 H compared with WT H (p < 0.05). The femur showed increased Tb.Sp for AT1 H and AT2 H, p < 0.01 and p < 0.05, respectively. The Tb.N was decreased in the vertebra (WT H-AT1 H: p < 0.05; WT H-AT2 H: p < 0.05) and in the femur (WT H-AT1 H: p < 0.01; WT H-AT2 H: p < 0.05). AT1 PD increased linear bone loss (p < 0.05) and decreased osteoblast cells (p < 0.05). RANKL immunostaining was intense for AT1 PD and WT PD (p < 0.001). OPG was intense in the WT H, WT PD, and AT2 PD when compared to AT1 PD (p < 0.001). AT1 PD showed weak immunostaining for osteocalcin compared with WT H, WT PD, and AT2 PD (p < 0.001). AT1 H showed significantly stronger immunostaining for osteonectin in fibroblasts compared to AT2 H (p < 0.01). Conclusion: AT1 receptor knockout changed bone density, the quality and number of bone trabeculae, decreased the number of osteoblast cells, and increased osteonectin in fibroblasts. Full article

(This article belongs to the Special Issue Molecular Mechanisms of Periodontal Disease 2.0)

► Show Figures

Figure 1

12 pages, 2193 KiB

Open AccessArticle

IL-8 as a Potential Therapeutic Target for Periodontitis and Its Inhibition by Caffeic Acid Phenethyl Ester In Vitro

by Yung-Kai Huang, Kuo-Feng Tseng, Ping-Hsuan Tsai, Jie-Sian Wang, Chang-Yu Lee and Ming-Yi Shen

Int. J. Mol. Sci. 2021, 22(7), 3641; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22073641 - 31 Mar 2021

Cited by 16 | Viewed by 2577

Abstract

Salivary levels of interleukin-8 (IL-8) are elevated in patients with periodontitis. Caffeic acid phenethyl ester (CAPE) improves the periodontal status in subjects. However, whether CAPE can reduce IL-8 expression is unclear. We collected saliva to determine proinflammatory cytokine levels and used subgingival calculus and surrounding tissues from patients with periodontitis for oral microbiota analysis via 16s ribosomal RNA gene sequencing. THP-1 cells were stimulated with sterile-filtered saliva from patients, and target gene/protein expression was assessed. IL-8 mRNA expression was analyzed in saliva-stimulated THP-1 cells treated with CAPE and the heme oxygenase-1 (HO-1) inhibitor tin-protoporphyrin (SnPP). In 72 symptomatic individuals, IL-8 was correlated with periodontal inflammation (bleeding on probing, r = 0.45; p < 0.001) and disease severity (bleeding on probing, r = 0.45; p < 0.001) but not with the four oral microbiota species tested. Reduced salivary IL-8 secretion was correlated with effective periodontitis treatment (r = 0.37, p = 0.0013). In THP-1 cells, saliva treatment induced high IL-8 expression and IKK2 and nuclear factor-κB (NF-κB) phosphorylation. However, the IKK inhibitor BMS-345541, NF-κB inhibitor BAY 11-7082, and CAPE attenuated saliva-induced IL-8 expression. CAPE induced HO-1 expression and inhibited IKK2, IκBα, and NF-κB phosphorylation. Blocking HO-1 decreased the anti-inflammatory activity of CAPE. The targeted suppression of IL-8 production using CAPE reduces inflammation and periodontitis. Full article

(This article belongs to the Special Issue Molecular Mechanisms of Periodontal Disease 2.0)

► Show Figures

Figure 1

Review

Jump to: Research

14 pages, 1058 KiB

Open AccessReview

Impact of Oral Microbiome in Periodontal Health and Periodontitis: A Critical Review on Prevention and Treatment

by Mattia Di Stefano, Alessandro Polizzi, Simona Santonocito, Alessandra Romano, Teresa Lombardi and Gaetano Isola

Int. J. Mol. Sci. 2022, 23(9), 5142; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23095142 - 05 May 2022

Cited by 46 | Viewed by 7216

Abstract

The skin, oral cavity, digestive and reproductive tracts of the human body harbor symbiotic and commensal microorganisms living harmoniously with the host. The oral cavity houses one of the most heterogeneous microbial communities found in the human organism, ranking second in terms of species diversity and complexity only to the gastrointestinal microbiota and including bacteria, archaea, fungi, and viruses. The accumulation of microbial plaque in the oral cavity may lead, in susceptible individuals, to a complex host-mediated inflammatory and immune response representing the primary etiological factor of periodontal damage that occurs in periodontitis. Periodontal disease is a chronic inflammatory condition affecting about 20–50% of people worldwide and manifesting clinically through the detection of gingival inflammation, clinical attachment loss (CAL), radiographic assessed resorption of alveolar bone, periodontal pockets, gingival bleeding upon probing, teeth mobility and their potential loss in advanced stages. This review will evaluate the changes characterizing the oral microbiota in healthy periodontal tissues and those affected by periodontal disease through the evidence present in the literature. An important focus will be placed on the immediate and future impact of these changes on the modulation of the dysbiotic oral microbiome and clinical management of periodontal disease. Full article

(This article belongs to the Special Issue Molecular Mechanisms of Periodontal Disease 2.0)

► Show Figures

Figure 1

21 pages, 604 KiB

Open AccessReview

Association between Maternal Periodontitis and Development of Systematic Diseases in Offspring

by Anna Starzyńska, Piotr Wychowański, Maciej Nowak, Bartosz Kamil Sobocki, Barbara Alicja Jereczek-Fossa and Monika Słupecka-Ziemilska

Int. J. Mol. Sci. 2022, 23(5), 2473; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23052473 - 24 Feb 2022

Cited by 8 | Viewed by 3304

Abstract

Periodontal disease (PD) is one of the most common oral conditions affecting both youths and adults. There are some research works suggesting a high incidence of PD in pregnant women. As an inflammatory disease of bacterial origin, PD may result in the activation of the pathways affecting the course and the pregnancy outcome. The authors, based on the literature review, try to answer the PICO question: Does maternal periodontitis (exposure) influence the incidence of complications rates in pregnancy and the development of systemic diseases in childhood and adult offspring (outcome) in the humans of any race (population) compared to the offspring of mothers with healthy periodontium (comparison)? The authors try to describe the molecular pathways and mechanisms of these interdependencies. There is some evidence that maternal periodontitis may affect the pregnancy course and outcome, resulting in preeclampsia, preterm delivery, vulvovaginitis and low birth weight. It can be suggested that maternal periodontitis may affect offspring epigenome and result in some health consequences in their adult life. Full article

(This article belongs to the Special Issue Molecular Mechanisms of Periodontal Disease 2.0)

► Show Figures

Figure 1

26 pages, 1902 KiB

Open AccessReview

A Narrative Review on Oral and Periodontal Bacteria Microbiota Photobiomodulation, through Visible and Near-Infrared Light: From the Origins to Modern Therapies

by Andrea Amaroli, Silvia Ravera, Angelina Zekiy, Stefano Benedicenti and Claudio Pasquale

Int. J. Mol. Sci. 2022, 23(3), 1372; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23031372 - 25 Jan 2022

Cited by 21 | Viewed by 4563

Abstract

Photobiomodulation (PBM) consists of a photon energy transfer to the cell, employing non-ionizing light sources belonging to the visible and infrared spectrum. PBM acts on some intrinsic properties of molecules, energizing them through specific light wavelengths. During the evolution of life, semiconducting minerals were energized by sun radiation. The molecules that followed became photoacceptors and were expressed into the first proto-cells and prokaryote membranes. Afterward, the components of the mitochondria electron transport chain influenced the eukaryotic cell physiology. Therefore, although many organisms have not utilized light as an energy source, many of the molecules involved in their physiology have retained their primordial photoacceptive properties. Thus, in this review, we discuss how PBM can affect the oral microbiota through photo-energization and the non-thermal effect of light on photoacceptors (i.e., cytochromes, flavins, and iron-proteins). Sometimes, the interaction of photons with pigments of an endogenous nature is followed by thermal or photodynamic-like effects. However, the preliminary data do not allow determining reliable therapies but stress the need for further knowledge on light-bacteria interactions and microbiota management in the health and illness of patients through PBM. Full article

(This article belongs to the Special Issue Molecular Mechanisms of Periodontal Disease 2.0)

► Show Figures

Figure 1

23 pages, 1512 KiB

Open AccessReview

Molecular Mechanisms Leading from Periodontal Disease to Cancer

by Bartosz Kamil Sobocki, Charbel A. Basset, Bożena Bruhn-Olszewska, Paweł Olszewski, Olga Szot, Karolina Kaźmierczak-Siedlecka, Mateusz Guziak, Luigi Nibali and Angelo Leone

Int. J. Mol. Sci. 2022, 23(2), 970; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23020970 - 16 Jan 2022

Cited by 13 | Viewed by 4036

Abstract

Periodontitis is prevalent in half of the adult population and raises critical health concerns as it has been recently associated with an increased risk of cancer. While information about the topic remains somewhat scarce, a deeper understanding of the underlying mechanistic pathways promoting neoplasia in periodontitis patients is of fundamental importance. This manuscript presents the literature as well as a panel of tables and figures on the molecular mechanisms of Porphyromonas gingivalis and Fusobacterium nucleatum, two main oral pathogens in periodontitis pathology, involved in instigating tumorigenesis. We also present evidence for potential links between the RANKL–RANK signaling axis as well as circulating cytokines/leukocytes and carcinogenesis. Due to the nonconclusive data associating periodontitis and cancer reported in the case and cohort studies, we examine clinical trials relevant to the topic and summarize their outcome. Full article

(This article belongs to the Special Issue Molecular Mechanisms of Periodontal Disease 2.0)

► Show Figures

Figure 1

23 pages, 1334 KiB

Open AccessReview

Pyroptosis-Mediated Periodontal Disease

by Mariane Beatriz Sordi, Ricardo de Souza Magini, Layla Panahipour and Reinhard Gruber

Int. J. Mol. Sci. 2022, 23(1), 372; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23010372 - 29 Dec 2021

Cited by 36 | Viewed by 4679

Abstract

Pyroptosis is a caspase-dependent process relevant to the understanding of beneficial host responses and medical conditions for which inflammation is central to the pathophysiology of the disease. Pyroptosis has been recently suggested as one of the pathways of exacerbated inflammation of periodontal tissues. Hence, this focused review aims to discuss pyroptosis as a pathological mechanism in the cause of periodontitis. The included articles presented similarities regarding methods, type of cells applied, and cell stimulation, as the outcomes also point to the same direction considering the cellular events. The collected data indicate that virulence factors present in the diseased periodontal tissues initiate the inflammasome route of tissue destruction with caspase activation, cleavage of gasdermin D, and secretion of interleukins IL-1β and IL-18. Consequently, removing periopathogens’ virulence factors that trigger pyroptosis is a potential strategy to combat periodontal disease and regain tissue homeostasis. Full article

(This article belongs to the Special Issue Molecular Mechanisms of Periodontal Disease 2.0)

► Show Figures

Figure 1

Journal Menu

Journal Browser

Molecular Mechanisms of Periodontal Disease 2.0

Share This Special Issue

Special Issue Editor

Special Issue Information

Keywords

Related Special Issues

Published Papers (11 papers)

Research

Review

Further Information

Guidelines

MDPI Initiatives

Follow MDPI