About this Research Topic
Adult periodontitis (PD) is a chronic inflammatory disease of aging or inflammaging. This is particularly striking when the NHANES data from 2009-2010 are stratified by patient age, with PD prevalence increasing from 24.4% in those 30-34 years of age to 70.1% in those 65 years and older. The co-morbidity of PD with other more serious age-related diseases is well known, but the underlying mechanisms are unclear. With advanced age comes an increase in accumulation of senescent cells, through cellular senescence (CS). Originally recognized as cell cycle arrest, CS has emerged as a causative factor in peripheral inflammation, impaired wound healing, and impaired immune-surveillance. PD and its co-morbid diseases will continue to grow unless innovative strategies are developed for early detection of senescent cells and the factors that induce them. This will lead to interventional tactics to eliminate senescent cells and improve the health and longevity of aged adults.
The goal of this Research Topic is to provide a contemporary inquiry of the role of immune senescence in age-related diseases such as periodontitis (PD) from a pathophysiological standpoint. This includes identification of molecular mechanisms involved, factors that can accelerate premature senescence in PD and crosstalk between innate/adaptive immune cells and non-immune cells. Recent advances in interventional tactics to eliminate senescent cells and improve the health and longevity of aged adults is a particularly relevant outcome.
The overall scope of this research in humans and animal models is on the role of advanced age and other pathophysiological factors, including oral microbes, in the induction of immune senescence in PD. In this regard, the early detection of immune senescence, the factors that accelerate premature senescence, the innate/adaptive arms of the immune response and the mediators of crosstalk between immune and non-immune cells are of interest. Both focused review articles and original articles that identify novel molecular mechanisms for the identification, induction and elimination of immune senescence are encouraged.
Keywords: cellular senescence, immune senescence, macrophages, dendritic cells, epithelial cells, myeloid derived suppressor cells, SASP, exosomes, inflammasome, Porphyromonas gingivalis, Fusobacterium nucleatum
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