Perio-Inflammation in Auto-Antibodies and T-Cell Mediated Oro-Pharyngeal Mucositis

A special issue of Journal of Clinical Medicine (ISSN 2077-0383).

Deadline for manuscript submissions: closed (31 March 2021) | Viewed by 27658

Special Issue Editors


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Guest Editor
Department of Neurosciences, Reproductive Science and Dentistry, Oral Medicine Unit, Federico II University of Naples, Via Pansini 5, 80138 Naples, Italy
Interests: oral cancer; oral potentially malignant disorders; erytroplakia; leukoplakia; oral lichen planus; autoimmune mucocutaneous bullous diseases; burning mouth syndrome
Special Issues, Collections and Topics in MDPI journals

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Guest Editor
Department of Neurosciences, Reproductive and Odontostomatological Sciences, University of Naples “Federico II”, 80131 Naples, Italy
Interests: oral medicine; dental materials; operative dentistry; oral health
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The ever-evolving literature on the role of chronic systemic inflammation in many systemic pathologies (cardiovascular diseases, preterm birth/low birth weight, obesity, diabetes, rheumatoid arthritis, Alzheimer's diseases) have shown a one-to-one correlation with chronic oral infections, and mainly with periodontal diseases. Chronic inflammation is characterized by an unlimited production of cytokines, growth factors and reactive oxygen/nitrogen compounds which, in the end, favor a "loss of function" following destruction, fibrosis and/or tissue and organ necrosis.

Periodontal inflammation is mainly mediated by neutrophils, monocytes/macrophages, T and B lymphocytes. The activation of the different T lymphocyte subgroups is crucial for the onset and progression of the periodontal lesion. Cytokines secreted by T lymphocytes can induce clonal activation of B lymphocytes, which act as APC cells and produce antibodies that recognize bacterial components, protecting periodontal tissues, however, the release of autoantibodies directed against collagen, fibronectin and laminin can, in turn, contribute to the local destruction of the gum tissue.

The complex mechanism and interaction between T and B cells in extra-oral sites are respectively the pathogenetic processes of two large groups of chronic diseases with oral involvement or with a rapid onset on the oral mucosa: blistering oro-pharyngeal IgG/IgA mediated diseases (Pemphigus vulgaris, Mucous Membrane Pemphigoid, IgA disease, Multiform Erythema are the most frequent) and cell-mediated interface mucositis (True Lichen Planus, drug-related lichenoid lesions, Graft versus host disease oral lichenoid lesions, Lupus Systemic Erythematous lichenoid lesions and Oral Dysplasia are the most frequent).

We particularly welcome articles providing new insights into (i) clinical/lab researches on the the correlation between periodontal diseases and T and B cell-mediated diseases; (ii) perio inflammation index evaluations in T and B cell-mediated diseases; (iii) clinical management of patients with T or B mediated perio/mucositis inflammation.

We welcome both solicited and unsolicited submissions that will contribute to this goal.

Prof. Dr. Stefania Leuci
Prof. Dr. Gianrico Spagnuolo
Guest Editors

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Keywords

  • Periodontal disease
  • Mucositis
  • Autoimmunity
  • Lichenoid lesions
  • Lichen planus
  • T lymphocytes
  • B lymphocytes
  • Pemphigus vulgaris
  • Mucous membrane pemphigoid

Published Papers (3 papers)

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11 pages, 58203 KiB  
Article
Clinico-Pathological Profile and Outcomes of 45 Cases of Plasma Cell Gingivitis
by Stefania Leuci, Noemi Coppola, Nicola Adamo, Maria Eleonora Bizzoca, Daniela Russo, Gianrico Spagnuolo, Lorenzo Lo Muzio and Michele Davide Mignogna
J. Clin. Med. 2021, 10(4), 830; https://doi.org/10.3390/jcm10040830 - 18 Feb 2021
Cited by 13 | Viewed by 9002
Abstract
Plasma cell gingivitis (PCG) is an infrequent inflammatory disease of the gingiva of unknown etiology, characterized by a dense polyclonal proliferation of plasma cells in the connective tissue. The aim of this study was to present a case series of patients affected by [...] Read more.
Plasma cell gingivitis (PCG) is an infrequent inflammatory disease of the gingiva of unknown etiology, characterized by a dense polyclonal proliferation of plasma cells in the connective tissue. The aim of this study was to present a case series of patients affected by PCG, analyzing demographic, clinical, histopathological, and therapeutic data. A group of 36 females and 9 males with a mean age of 60.3 years was evaluated. Clinically, 25 cases were bullous, a clinical phenotype never reported to date, 4 erythematous, 4 keratotic, 4 verruciform, and 3 ulcerative. On histological examination, pure polyclonal plasma cell infiltrate was detected in 20 specimens, while in 25 specimens it was associated with a mixed infiltrate. The first-line therapy consisted of oral hygiene and topical corticosteroids in all patients. In 25 patients, doxycycline and sulfasalazine were added; in 10 of these patients, the disease persisted, and it was necessary to resort to systemic steroids. This study presented the clinico-pathological profile and outcomes of a case series of PCG. This could be an aid for clinicians to be aware of the heterogeneous clinical phenotype and of the possible pure bullous phenotype of PCG. Further studies are needed to improve the knowledge about this disorder. Full article
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Review

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14 pages, 1058 KiB  
Review
Predictive Periodontitis: The Most Promising Salivary Biomarkers for Early Diagnosis of Periodontitis
by Carlo Cafiero, Gianrico Spagnuolo, Gaetano Marenzi, Ranieri Martuscelli, Michele Colamaio and Stefania Leuci
J. Clin. Med. 2021, 10(7), 1488; https://doi.org/10.3390/jcm10071488 - 03 Apr 2021
Cited by 35 | Viewed by 6260
Abstract
The primary cause of tooth loss in the industrialized world is periodontitis, a bacterial anaerobic infection whose pathogenesis is characterized by composite immune response. At present, the diagnose of periodontitis is made by a complete status check of the patient’s periodontal health; full-mouth [...] Read more.
The primary cause of tooth loss in the industrialized world is periodontitis, a bacterial anaerobic infection whose pathogenesis is characterized by composite immune response. At present, the diagnose of periodontitis is made by a complete status check of the patient’s periodontal health; full-mouth plaque score, full-mouth bleeding score, probing depth, clinical attachment level, bleeding on probing, recessions, mobility, and migration are evaluated in order to provides a clear picture of the periodontal conditions of a single patient. Chair-side diagnostic tests based on whole saliva could be routinely used by periodontists for a very early diagnosis of periodontitis, monitoring, prognosis, and management of periodontal patients by biomarker detection, whose diagnostic validity is related to sensitivity and specificity. Recent paper reviews and meta-analyses have focused on five promising host derived biomarkers as candidate for early diagnosis of periodontitis: MMP-8 (Metalloproteinase-8), MIP-1α (Macrophage inflammatory protein-1 alpha), IL-1 β (Interleukin-1 beta), IL-6 (Interleukin-6), and HB (Hemoglobin), and their combinations. Chair-side Lab-on-a-chip (LOC) technology may soon become an important part of efforts to detect such biomarkers in saliva medium to improve worldwide periodontal health in developed nations as well as in underserved communities and poor countries. Their applications in preventive and predictive medicine is now fundamental, and is aimed at the early detection of risk factors or the presence or evolution of the disease, and in personalized medicine, which aims to identify tailor-made treatments for individual patients. The aim of the present paper is to be informative about host derived periodontal biomarkers and, in particular, we intend to report information about the most important immune response derived biomarkers and Hemoglobin as candidates to be routinely utilized in order to obtain a chair-side early diagnosis of periodontal disease. Full article
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21 pages, 424 KiB  
Review
The Role of Periodontitis and Periodontal Bacteria in the Onset and Progression of Alzheimer’s Disease: A Systematic Review
by Mario Dioguardi, Vito Crincoli, Luigi Laino, Mario Alovisi, Diego Sovereto, Filiberto Mastrangelo, Lucio Lo Russo and Lorenzo Lo Muzio
J. Clin. Med. 2020, 9(2), 495; https://doi.org/10.3390/jcm9020495 - 11 Feb 2020
Cited by 90 | Viewed by 10750
Abstract
The evidence of a connection between the peripheral inflammatory processes and neurodegenerative diseases of the central nervous system is becoming more apparent. This review of the related literature highlights the most recent clinical, epidemiological, and in vitro studies trying to investigate possible connections [...] Read more.
The evidence of a connection between the peripheral inflammatory processes and neurodegenerative diseases of the central nervous system is becoming more apparent. This review of the related literature highlights the most recent clinical, epidemiological, and in vitro studies trying to investigate possible connections between periodontal bacteria and the onset and progression of Alzheimer’s disease. This review was conducted by searching databases such as PubMed and Scopus using keywords or combinations such as Alzheimer’s Disease AND periodontal or dementia AND periodontitis OR periodontal. After eliminating overlaps and screening the articles not related to these issues, we identified 1088 records and proceeded to the selection of articles for an evaluation of the associative assumptions. The hypothesis suggested by the authors and confirmed by the literature is that the bacterial load and the inflammatory process linked to periodontal disease can intensify inflammation at the level of the central nervous system, favoring the occurrence of the disease. The analysis of the literature highlights how periodontal disease can directly contribute to the peripheral inflammatory environment by the introduction of periodontal or indirect pathogenic bacteria and proinflammatory cytokines locally produced at the periodontal level following bacterial colonization of periodontal defects. Full article
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