Chemokine Function in Periodontal Disease and Oral Cavity Cancer

Abstract

The chemotactic cytokines, or chemokines, comprise a superfamily of polypeptides with a wide range of activities that include recruitment of immune cells to sites of infection and inflammation, as well as stimulation of cell proliferation. As such, they function as antimicrobial molecules and play a central role in host defenses against pathogen challenge. However, their ability to recruit leukocytes and potentiate or prolong the inflammatory response may have profound implications for the progression of oral diseases such as chronic periodontitis, where tissue destruction may be widespread. Moreover, it is increasingly recognized that chronic inflammation is a key component of tumor progression. Interaction between cancer cells and their microenvironment is mediated in large part by secreted factors such as chemokines, and serves to enhance the malignant phenotype in oral and other cancers. In this article, we will outline the biological and biochemical mechanisms of chemokine action in host–microbiome interactions in periodontal disease and in oral cancer, and how these may overlap and contribute to pathogenesis.

Microbiota, cirrhosis, and the emerging oral-gut-liver axis

“…The proposed mechanisms linking periodontal disease and systemic conditions include shared risk factors, direct effects of oral bacteria, and continuous exposure to inflammatory mediators. Besides local tissue effects, periodontitis is also associated with increased risk of several systemic conditions, such as diabetes, cardiovascular and respiratory diseases, pregnancy complications, cancer, and possibly liver diseases (71)(72)(73)(74)(75). Therefore, the tightly regulated interaction between the oral microbiota and the host immune system within the oral mucosa is key for maintaining tissue homeostasis and preventing adverse clinical outcomes.…”

Insights into the Evolution of Host Association through the Isolation and Characterization of a Novel Human Periodontal Pathobiont,Desulfobulbus oralis

“…During the initial stages of periodontal disease, there is an acute inflammatory response to some of the oral microbiota resulting in the recruitment of polymorphonuclear leukocytes stimulated by host chemokines and/or cytokines, such as interleukin-8 (IL-8) (86). As inflammation progresses from acute to chronic, an increase in the production of proinflammatory mediators such as IL-1␤, IL-6, IL-8, and tumor necrosis factor alpha (TNF-␣) by various host cells, including oral epithelial keratinocytes, results in the recruitment of additional immune cells such as macrophages, T cells, and B cells (86). There is still insufficient data to distinguish the relative roles of oral bacterial lipopolysaccharide (LPS) and surface-associated and secreted proteins in cytokine induction.…”

Interplay of Toll-Like Receptor 9, Myeloid Cells, and Deubiquitinase A20 in Periodontal Inflammation

“…Periodontitis is one of the most prevalent oral diseases, affecting almost half of the American population, and is associated with increased risk of systemic conditions, including diabetes, cardiovascular disease, cancer, adverse pregnancy outcomes, gastrointestinal and pulmonary diseases, and rheumatoid arthritis (9)(10)(11)(12)(13)(14)(15). While periodontal diseases are initiated by periodontopathic bacteria and dysbiosis, the deregulated host inflammatory response to this dysbiotic microflora leads to destruction of the tooth supporting structures and eventual tooth loss (16).…”