Periodontal Disease and Senescent Cells: New Players for an Old Oral Health Problem?
Periodontal Disease and Senescent Cells: New Players for an Old Oral Health Problem?
复制标题
牙周疾病和衰老细胞：旧口腔健康问题的新参与者？
DOI：
10.3390/ijms21207441
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发表时间：
2020-10-09
影响因子：
5.6
通讯作者：
Monroe DG
中科院分区：
文献类型：
--
作者：
Aquino-Martinez R;Khosla S;Farr JN;Monroe DG
最近在牙周组织中发现的衰老细胞有可能为牙周病病因学的潜在机制提供新的见解。DNA损伤驱动的衰老可能是持续性革兰氏阴性细菌感染和炎症的最被低估的延迟后果之一。虽然宿主的免疫反应可以迅速防止细菌入侵，但炎症过程中产生的氧化应激可以通过损伤重要的细胞大分子（包括DNA）间接恶化牙周组织。那些生活在有害环境中的健康细胞会发生什么？新出现的证据表明，在不可修复的基因组损伤中存活下来的细胞会经历细胞衰老，这是连接DNA损伤和免疫反应的关键中间机制。在这篇综述中，我们假设，持续的革兰氏阴性细菌的挑战，慢性炎症本身，以及受损组织的不断更新，为衰老细胞的异常积累创造了一个宽松的环境。基于新出现的数据，我们提出了一个模型，其中衰老细胞的功能失调可能会加剧对病原体的初始免疫反应。进一步了解衰老细胞在牙周病发病机制中的作用，可能会提供更复杂的治疗策略，以打击组织破坏的临床意义。
The recent identification of senescent cells in periodontal tissues has the potential to provide new insights into the underlying mechanisms of periodontal disease etiology. DNA damage-driven senescence is perhaps one of the most underappreciated delayed consequences of persistent Gram-negative bacterial infection and inflammation. Although the host immune response rapidly protects against bacterial invasion, oxidative stress generated during inflammation can indirectly deteriorate periodontal tissues through the damage to vital cell macromolecules, including DNA. What happens to those healthy cells that reside in this harmful environment? Emerging evidence indicates that cells that survive irreparable genomic damage undergo cellular senescence, a crucial intermediate mechanism connecting DNA damage and the immune response. In this review, we hypothesize that sustained Gram-negative bacterial challenge, chronic inflammation itself, and the constant renewal of damaged tissues create a permissive environment for the abnormal accumulation of senescent cells. Based on emerging data we propose a model in which the dysfunctional presence of senescent cells may aggravate the initial immune reaction against pathogens. Further understanding of the role of senescent cells in periodontal disease pathogenesis may have clinical implications by providing more sophisticated therapeutic strategies to combat tissue destruction.
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