Abstract
Chronic apical periodontitis (CAP) is a unique dynamic interaction between microbial invasions and host defense mechanisms, resulting in infiltration of immune cells, bone absorption, and periapical granuloma formation. To help to understand periapical tissue pathophysiology, we constituted a single-cell atlas for 26,737 high-quality cells from inflammatory periapical tissue and uncovered the complex cellular landscape. The eight types of cells, including nonimmune cells and immune cells, were identified in the periapical tissue of CAP. Considering the key roles of nonimmune cells in CAP, we emphasized osteo-like cells, basal/stromal cells, endothelial cells, and epithelial cells, and discovered their diversity and heterogeneity. The temporal profiling of genomic alterations from common CAP to typical periapical granuloma provided predictions for transcription factors and biological processes. Our study presented potential clues that the shift of inflammatory cytokines, chemokines, proteases, and growth factors initiated polymorphic cell differentiation, lymphangiogenesis, and angiogenesis during CAP.
Highlights
Chronic apical periodontitis (CAP), caused by bacterial infection, is the most frequent tooth disease in the jaws, and manifested as periapical tissue destruction, alveolar bone resorption, and inflammatory granulation tissue formation (Chan et al, 2013)
Though human teeth had been mapped the transcriptional landscape of the various cell populations at single-cell resolution (Krivanek et al, 2020; Pagella et al, 2021), to our knowledge, cellular heterogeneity in lesions of human CAP has not been studied hitherto
Inflammatory granulation tissue formation, and alveolar bone resorption are the hallmarks of CAP
Summary
Chronic apical periodontitis (CAP), caused by bacterial infection, is the most frequent tooth disease in the jaws, and manifested as periapical tissue destruction, alveolar bone resorption, and inflammatory granulation tissue formation (Chan et al, 2013). CAP is an inflammatory disease caused by the complex interaction between various types of cellular compositions in periapical lesions, comprising immune cells and nonimmune cells. The aberrant proliferation of immune cells interferes with the established cellular equilibrium in the lesion, and drives a detrimental inflammatory response to impair periapical tissue. The histological identification of inflammatory cells has highlighted the roles of immune cells, little is known about the molecular mechanism of nonimmune cells in CAP at the single-cell level. The recent widespread use of single-cell and high-throughput sequencing in many fields provided an opportunity to comprehensively understand cellular heterogeneity and multiple biological processes of nonimmune cells in odontogenic CAP. Lymphangiogenesis and angiogenesis were predicted by the abnormal activation of endothelial cells and regulatory program, which implied immunological feedback from the host system in CAP
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