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Introduction
Chronic inflammation has been associated with several disease conditions ranging from metabolic, autoimmune, cardiopulmonary, and neurodegenerative diseases. The inflammatory process is a progressive one that can trigger the malignant transformation of cells in the vicinity, thereby supporting the pathways related to carcinogenesis. Escalating trends of cancer, especially head and neck, lung, and colon cancer in the South Asian population, is bewildering. Although several risk factors have been identified in relation to these phenotypes, the development of cancer in young adults with no exposure to habits like tobacco usage, smoking, or alcoholism raises questions about the mechanisms underlying the process of carcinogenesis [1, 2–3]. While probing extensively into the converging factors, inflammation and oral hygiene were closely associated with the malignant transformation of epithelial cells. The dysbiosis of the oral microbiome in metabolic disorders has been considered a significant risk factor that causes normal cells to acquire an abnormal phenotype [4]. Various genetic and epigenetic mechanisms have been recognized as key contributors to the development of oral cancer [5, 6]. Very recently, epi-transcriptomic factors, such as readers, erasers, and writers, that identify, remove, or add methylation marks to RNA molecules, respectively, were found to control the expression profile of a candidate gene intricately [7]. Overall, periodontitis (PD), a chronic inflammatory disease affecting the oral cavity, has been identified as a possible risk factor for cancer. In line with this concept, PD was chosen for further investigation as it is a common, complex multifactorial trait with high prevalence.
The genomic, epigenomic, transcriptomic, and proteomic signatures of periodontal disease and cancer have been reported by numerous researchers. The local inflammatory response elicited during PD interferes with the normal cellular processes, promoting proliferation and invasion of cancer cells. During PD, the periodontium undergoes phenotypic and functional changes, creating a tumor-supportive microenvironment that promotes cancer progression. The buildup of such an inflammasome milieu provides a conducive environment for seeding tumor cells, evading immune recognition, uncontrolled proliferation, and migration [8]. Wadia’s systematic review and meta-analysis revealed a strong correlation between PD and lung cancer [9]. Despite these facts, lacunae exist in sorting or identifying genetic markers common to both disease phenotypes. The present study is an attempt to delineate those differentially expressed genes of the periodontitis group and compare their...