Abstract
Periodontitis (PD) is increasingly considered to interact with and promote a number of inflammatory diseases, including cancer. In the case of oral squamous cell carcinoma (OSCC) the local inflammatory response associated with PD is capable of triggering altered cellular events that can promote cancer cell invasion and proliferation of existing primary oral carcinomas as well as supporting the seeding of metastatic tumor cells into the gingival tissue giving rise to secondary tumors. Both the immune and stromal components of the periodontium exhibit phenotypic alterations and functional differences during PD that result in a microenvironment that favors cancer progression. The inflammatory milieu in PD is ideal for cancer cell seeding, migration, proliferation and immune escape. Understanding the interactions governing this attenuated anti-tumor immune response is vital to unveil unexplored preventive or therapeutic possibilities. Here we review the many commonalities between the oral-inflammatory microenvironment in PD and oral-inflammatory responses that are associated with OSCC progression, and how these conditions can act to promote and sustain the hallmarks of cancer.
Highlights
Periodontitis (PD) is increasingly considered to interact with and promote a number of inflammatory diseases, including cancer
Th17 cells have been linked to unfavorable prognostic outcomes in patients with cancer in the head and neck region [157]. This may come as a result of the tumor promoting activities of IL-17, which regulates the levels of vascular endothelial growth factor (VEGF)-A and IL-6 promoting the proliferation of oral cancer cell [157]
In an era where understanding the putative interconnectivity between cancer and other diseases, inflammatory diseases, unveils new aspects and targets for cancer therapy, it has become clear that PD has the potential to exacerbate all the pathogenic characteristics of oral squamous cell carcinoma (OSCC)
Summary
In relation to the above, the putative role played by inflammation in tumourigenesis can be observed in the oral cavity [3]. An association between PD and OSCC, two conditions that co-exist within the oral microenvironment, has been confirmed in many studies, suggesting that the immunologically distinct oral setting in PD could support tumor progression [14, 15] Based on this observation one might reasonably predict that the most common site of primary squamous cell carcinomas in the oral cavity will be the gingival tissue, from which periodontal disease arises, this was found not to be the case. Periodontal pathogen P. gingivalis is able to stimulate the expression of the CXCL14 from oral epithelial cells both directly and by antagonizing epidermal growth factor (EGF)induced activation of the MEK-ERK1/2 pathway known to repress CXCL14 transcription [44] This CXCL14 involvement in PD may be considered as one of the methods by which antitumor responses are supported. Further research will be necessary to understand the complex interactions between PD and OSCC
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