Periodontitis and oral cancer - current concepts of the etiopathogenesis

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Abstract

Gingival tissues are attacked by oral pathogens which can induce inflammatory reactions. The immune-inflammatory responses play essential roles in the patient susceptibility to periodontal diseases. There is a wealth of evidence indicating a link between chronic inflammation and risk of malignant transformation of the affected oral epithelium. Periodontitis is associated with an increased risk of developing chronic systemic conditions including autoimmune diseases and different types of cancers. Besides, some risk factors such as smoking, alcohol consumption and human papilloma virus have been found to be associated with both periodontitis and oral cancer. This review article aimed to study the current concepts in pathogenesis of chronic periodontitis and oral cancer by reviewing the related articles.

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Role of Human Macrophage Polarization in Inflammation during Infectious Diseases

Chiraz Atri, Fatma Z. Guerfali, Dhafer Laouini (2018)

Experimental models have often been at the origin of immunological paradigms such as the M1/M2 dichotomy following macrophage polarization. However, this clear dichotomy in animal models is not as obvious in humans, and the separating line between M1-like and M2-like macrophages is rather represented by a continuum, where boundaries are still unclear. Indeed, human infectious diseases, are characterized by either a back and forth or often a mixed profile between the pro-inflammatory microenvironment (dominated by interleukin (IL)-1β, IL-6, IL-12, IL-23 and Tumor Necrosis Factor (TNF)-α cytokines) and tissue injury driven by classically activated macrophages (M1-like) and wound healing driven by alternatively activated macrophages (M2-like) in an anti-inflammatory environment (dominated by IL-10, Transforming growth factor (TGF)-β, chemokine ligand (CCL)1, CCL2, CCL17, CCL18, and CCL22). This review brews the complexity of the situation during infectious diseases by stressing on this continuum between M1-like and M2-like extremes. We first discuss the basic biology of macrophage polarization, function, and role in the inflammatory process and its resolution. Secondly, we discuss the relevance of the macrophage polarization continuum during infectious and neglected diseases, and the possibility to interfere with such activation states as a promising therapeutic strategy in the treatment of such diseases.

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Obesity and Cancer Mechanisms: Tumor Microenvironment and Inflammation

Neil M Iyengar, Clifford Hudis, Andrew Dannenberg … (2016)

Purpose There is growing evidence that inflammation is a central and reversible mechanism through which obesity promotes cancer risk and progression. Methods We review recent findings regarding obesity-associated alterations in the microenvironment and the local and systemic mechanisms through which these changes support tumor growth. Results Locally, hyperadiposity is associated with altered adipose tissue function, adipocyte death, and chronic low-grade inflammation. Most individuals who are obese harbor inflamed adipose tissue, which resembles chronically injured tissue, with immune cell infiltration and remodeling. Within this distinctly altered local environment, several pathophysiologic changes are found that may promote breast and other cancers. Consistently, adipose tissue inflammation is associated with a worse prognosis in patients with breast and tongue cancers. Systemically, the metabolic syndrome, including dyslipidemia and insulin resistance, occurs in the setting of adipose inflammation and operates in concert with local mechanisms to sustain the inflamed microenvironment and promote tumor growth. Importantly, adipose inflammation and its protumor consequences can be found in some individuals who are not considered to be obese or overweight by body mass index. Conclusion The tumor-promoting effects of obesity occur at the local level via adipose inflammation and associated alterations in the microenvironment, as well as systemically via circulating metabolic and inflammatory mediators associated with adipose inflammation. Accurately characterizing the obese state and identifying patients at increased risk for cancer development and progression will likely require more precise assessments than body mass index alone. Biomarkers of adipose tissue inflammation would help to identify high-risk populations. Moreover, adipose inflammation is a reversible process and represents a novel therapeutic target that warrants further study to break the obesity-cancer link.

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The Roles of Autophagy in Cancer

Chul Yun, Sang Hun Lee (2018)

Autophagy is an intracellular degradative process that occurs under several stressful conditions, including organelle damage, the presence of abnormal proteins, and nutrient deprivation. The mechanism of autophagy initiates the formation of autophagosomes that capture degraded components and then fuse with lysosomes to recycle these components. The modulation of autophagy plays dual roles in tumor suppression and promotion in many cancers. In addition, autophagy regulates the properties of cancer stem-cells by contributing to the maintenance of stemness, the induction of recurrence, and the development of resistance to anticancer reagents. Although some autophagy modulators, such as rapamycin and chloroquine, are used to regulate autophagy in anticancer therapy, since this process also plays roles in both tumor suppression and promotion, the precise mechanism of autophagy in cancer requires further study. In this review, we will summarize the mechanism of autophagy under stressful conditions and its roles in tumor suppression and promotion in cancer and in cancer stem-cells. Furthermore, we discuss how autophagy is a promising potential therapeutic target in cancer treatment.

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Author and article information

Journal

Journal ID (nlm-ta): Oncol Rev

Journal ID (iso-abbrev): Oncol Rev

Journal ID (publisher-id): ONCOL

Title: Oncology Reviews

Publisher: PAGEPress Publications, Pavia, Italy

ISSN (Print): 1970-5565

ISSN (Electronic): 1970-5557

Publication date (Electronic): 18 March 2020

Publication date Collection: 18 February 2020

Volume: 14

Issue: 1

Electronic Location Identifier: 465

Affiliations

[1 ]Dental Research Centre, Oral Pathology Department, Dental Faculty, Hamadan University of Medical Sciences

[2 ]Department of Periodontology, Dental Faculty, Hamadan University of Medical Sciences

[3 ]Dental Student, Dental Faculty, Hamadan University of Medical Sciences , Hamadan, Iran

Author notes

Dental Faculty, Shahid Fahmideh Street, Hamadan, Iran. Postal code: 65178-38741. +98.813.8354250 - +98.813.8354220. sousanirani@ 123456gmail.com

Article

DOI: 10.4081/oncol.2020.465

PMC ID: 7097927

PubMed ID: 32231765

SO-VID: 74e9eeb6-0fbf-4323-86af-94860bff5950

License:

This article is distributed under the terms of the Creative Commons Attribution Noncommercial License ( by-nc 4.0) which permits any noncommercial use, distribution, and reproduction in any medium, provided the original author(s) and source are credited.

History

Date received : 27 November 2019

Date accepted : 12 February 2020

Page count

Figures: 1, Tables: 5, Equations: 0, References: 178, Pages: 12

Funding

Funding: the authors would like to thank Hamadan University of Medical Sciences for financial support.

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Periodontitis and oral cancer - current concepts of the etiopathogenesis

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Microbiota and Host

Most cited references 151

Role of Human Macrophage Polarization in Inflammation during Infectious Diseases

Obesity and Cancer Mechanisms: Tumor Microenvironment and Inflammation

The Roles of Autophagy in Cancer

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