Abstract
Senescent cells express a senescence-associated secretory phenotype (SASP) with a pro-inflammatory bias, which contributes to the chronicity of inflammation. During chronic inflammatory diseases, infiltrating CD4+ T lymphocytes can undergo cellular senescence and arrest the surface expression of CD28, have a response biased towards T-helper type-17 (Th17) of immunity, and show a remarkable ability to induce osteoclastogenesis. As a cellular counterpart, T regulatory lymphocytes (Tregs) can also undergo cellular senescence, and CD28− Tregs are able to express an SASP secretome, thus severely altering their immunosuppressive capacities. During periodontitis, the persistent microbial challenge and chronic inflammation favor the induction of cellular senescence. Therefore, senescence of Th17 and Treg lymphocytes could contribute to Th17/Treg imbalance and favor the tooth-supporting alveolar bone loss characteristic of the disease. In the present review, we describe the concept of cellular senescence; particularly, the one produced during chronic inflammation and persistent microbial antigen challenge. In addition, we detail the different markers used to identify senescent cells, proposing those specific to senescent T lymphocytes that can be used for periodontal research purposes. Finally, we discuss the existing literature that allows us to suggest the potential pathogenic role of senescent CD4+CD28− T lymphocytes in periodontitis.
Highlights
Introduction iationsPeriodontitis is the most prevalent osteolytic disease in humans in which factors directly related to aging significantly contribute to the development of the disease [1].During periodontitis, chronic inflammation in response to bacterial challenge leads to irreversible resorption of tooth-supporting alveolar bone and tooth loss [1,2]
This review aims summarize and discuss the evidence regarding pathogenic senescent CD4+ T lymphocytes as a potential mediator in the periodontal microenvironment that contributes to to summarize and discuss the evidence regarding pathogenic senescent CD4+ T lymphocytes as a potential mediator in the periodontal microenvironment that contributes to osteoimmunological changes responsible for alveolar bone loss, the Th17/T regulatory lymphocytes (Tregs) imbalance in periodontitis-affected tissues
The chronically inflamed periodontitis-affected tissues enriched in pro-inflammatory mediators favor the continuance of a deregulated immune response characterized by the Th17/Treg imbalance that leads to pathologic alveolar bone resorption
Summary
Periodontitis is the most prevalent osteolytic disease in humans in which factors directly related to aging significantly contribute to the development of the disease [1]. Chronic inflammation in response to bacterial challenge leads to irreversible resorption of tooth-supporting alveolar bone and tooth loss [1,2]. The development of periodontitis goes through three clearly established steps: (a) first, a polymicrobial synergy and dysbiosis of the subgingival microbiota, in which the periodontal bacteria with pathogenic potential accumulate, pass through the gingival epithelium, and invade the connective tissues, (b) second, the consequent development of periodontal inflammation in which the host immune response is triggered against the bacterial insult, (c) and periodontal tissue breakdown, which involves the destruction of the connective tissue attachment to the tooth and irreversible alveolar bone resorption [2].
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