Journal
FRONTIERS IN IMMUNOLOGY
Volume 13, Issue -, Pages -Publisher
FRONTIERS MEDIA SA
DOI: 10.3389/fimmu.2022.915081
Keywords
neutrophils; systemic inflammation; trained immunity; innate immune memory; periodontitis; periodontal disease; atherosclerosis; atherosclerotic cardiovascular disease
Categories
Funding
- UK National Institute for Health and Care Research
- US National Institutes of Health [DE031206]
- Indonesia Endowment Fund for Education (LPDP-Indonesia Scholarship) [S-1692/LPDP.4/2019]
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Inflammation plays a crucial role in the development of atherosclerosis, and periodontitis is linked to this chronic inflammatory disease. Neutrophils play an important role in mediating the relationship between periodontitis and atherosclerosis. Systemic inflammation triggered by periodontitis can lead to the overproduction and hyper-responsiveness of neutrophils, contributing to the progression of atherosclerosis.
Inflammation plays a crucial role in the onset and development of atherosclerosis. Periodontitis is a common chronic disease linked to other chronic inflammatory diseases such as atherosclerotic cardiovascular disease (ASCVD). The mechanistic pathways underlying this association are yet to be fully understood. This critical review aims at discuss the role of neutrophils in mediating the relationship between periodontitis and ASCVD. Systemic inflammation triggered by periodontitis could lead to adaptations in hematopoietic stem and progenitor cells (HSPCs) resulting in trained granulopoiesis in the bone marrow, thereby increasing the production of neutrophils and driving the hyper-responsiveness of these abundant innate-immune cells. These alterations may contribute to the onset, progression, and complications of atherosclerosis. Despite the emerging evidence suggesting that the treatment of periodontitis improves surrogate markers of cardiovascular disease, the resolution of periodontitis may not necessarily reverse neutrophil hyper-responsiveness since the hyper-inflammatory re-programming of granulopoiesis can persist long after the inflammatory inducers are removed. Novel and targeted approaches to manipulate neutrophil numbers and functions are warranted within the context of the treatment of periodontitis and also to mitigate its potential impact on ASCVD.
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