Abstract
Periodontitis is a highly prevalent chronic inflammatory disease leading to periodontal tissue breakdown and subsequent tooth loss, in which excessive host immune response accounts for most of the tissue damage and disease progression. Despite of the imperative need to develop host modulation therapy, the inflammatory responses and cell population dynamics which are finely tuned by the pathological microenvironment in periodontitis remained unclear. To investigate the local microenvironment of the inflammatory response in periodontitis, 10 periodontitis patients and 10 healthy volunteers were involved in this study. Single-cell transcriptomic profilings of gingival tissues from two patients and two healthy donors were performed. Histology, immunohistochemistry, and flow cytometry analysis were performed to further validate the identified cell subtypes and their involvement in periodontitis. Based on our single-cell resolution analysis, we identified HLA-DR-expressing endothelial cells and CXCL13+ fibroblasts which are highly associated with immune regulation. We also revealed the involvement of the proinflammatory NLRP3+ macrophages in periodontitis. We further showed the increased cell-cell communication between macrophage and T/B cells in the inflammatory periodontal tissues. Our data generated an intriguing catalog of cell types and interaction networks in the human gingiva and identified new inflammation-promoting cell subtypes involved in chronic periodontitis, which will be helpful in advancing host modulation therapy.
Highlights
Periodontitis, a chronic inflammatory lesion of the collective periodontium, is characterized by irreversible and progressive degradation of the periodontal tissue and causes tooth loss and alveolar bone defects
We identified that HLA-DR-expressing endothelial cells and CXCL13+ fibroblasts were highly associated with immune regulation
We present the transcriptomic profiling of a total of 29,967 single cells of human gingival tissue using the scRNA-seq method
Summary
Periodontitis, a chronic inflammatory lesion of the collective periodontium, is characterized by irreversible and progressive degradation of the periodontal tissue and causes tooth loss and alveolar bone defects. Current periodontal treatment approaches focusing primarily on biofilm reduction have shown insufficiency to result in clinical improvement and to prevent the relapse of the disease. It is well recognized that periodontitis results from dysbiosis and the dysregulation of immune homeostasis [4]. Several types of cells are included in the hosts’ armamentarium against dysbiosis, epithelial cells, endothelial cells, fibroblast cells, immune cells, and undifferentiated mesenchymal cells [5,6,7]. All these cells precisely orchestrate an appropriate response to the biofilm microorganism and its components. An inappropriate and excessive host response arises, resulting in collateral periodontal tissue damage
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