Apical periodontitis is an oral common inflammatory disease initiated by infection of pulp chamber and is characterized by destruction and resorption of the periapical bone. As a local infection, pathogens and their products in periapical tissues, as well as inflammatory cytokines produced in periapical lesions, enter the blood circulation, triggering systemic immune responses and leading to the pathogenesis of various types of systemic disease. Therefore, apical periodontitis might be associated with systemic disease rather than solely simple local oral disease. In addition, the existence of a hyperinflammatory state in certain patients with chronic inflammation-related disorder may affect the progression or prognosis of apical periodontitis. However, the association and potential mechanisms between apical periodontitis and systemic diseases remain unclear. An in-depth understanding of the association between apical periodontitis and systemic disease will be useful for both dentists and physicians to eliminate the possible risk factors and promote the healing of apical periodontitis and systemic disease. Thus, the aim of the present review is to introduce the potential relationship between apical periodontitis and systemic disease.

In recent years, circular RNAs (circRNAs) have been shown to have critical regulatory roles in cancer biology. However, the contributions of circRNAs to non-small cell lung cancer (NSCLC) remain largely unknown. Methods: circFNDC3B (a circRNA derived from the FNDC3B gene) was identified by RNA-sequencing and validated by quantitative reverse transcription PCR. The role of circFNDC3B in NSCLC progression was assessed both in vitro and in vivo. CircRNAs in vivo precipitation, RNA binding protein immunoprecipitation (RIP), luciferase reporter assay, chromatin Immunoprecipitation (ChIP) and fluorescence in situ hybridization (FISH) were conducted to evaluate the interaction between circFNDC3B-GTF2I complex and CXCL10 & CXCL11 promotors. Results: The expression of circFNDC3B was higher in NSCLC tissues. The upregulation of circFNDC3B in NSCLC was significantly negative correlated with CD8+ T cells infiltration and served as an independent risk factor for overall survival in patients with NSCLC after pneumonectomy. Our in vivo and in vitro data indicated that circFNDC3B suppressed CD8+ T cells infiltration in NSCLC. Mechanistically, we found that circFNDC3B could inhibit the expression of CXCL10 & CXCL11 by interacting with GTF2I, regulating the migration of activated CD8+ T cells. Conclusions: These results reveal an important role of circFNDC3B in the immune infiltration of NSCLC and provide a fresh perspective on circRNAs in NSCLC progression.

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