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Maintaining a protective state for human periodontal tissue
Periodontology 2000 ( IF 17.5 ) Pub Date : 2021-03-10 , DOI: 10.1111/prd.12367
Matsuo Yamamoto 1 , Ryo Aizawa 1
Affiliation  

Periodontitis, caused by infection with periodontal pathogens, is primarily characterized by inflammatory bone resorption and destruction of connective tissue. Simply describing periodontitis as a specific bacterial infection cannot completely explain the various periodontal tissue destruction patterns observed. Periodontal tissue damage is thought to be caused by various factors. In recent years, research goals for periodontal pathogens have shifted from searching for specific pathogens to investigating mechanisms that damage periodontal tissues. Bacteria interact directly with the host in several ways, influencing expression and activity of molecules that evade host defenses, and destroying local tissues and inhibiting their repair. The host's innate and acquired immune systems are important defense mechanisms that protect periodontal tissues from attack and invasion of periodontal pathogens, thus preventing infection. Innate and acquired immunity have evolved to confront the microbial challenge, forming a seamless defense network in periodontal tissues. In the innate immune response, host cells quickly detect, via specialized receptors, macromolecules and nucleic acids present on bacterial cell walls, and this triggers a protective, inflammatory response. The work of this subsystem of host immunity is performed mainly by phagocytes, beta‐defensin, and the complement system. In addition, the first line of defense in oral innate immunity is the junctional epithelium, which acts as a physical barrier to the entry of oral bacteria and other nonself substances. In the presence of a normal flora, junctional epithelial cells differentiate actively and proliferate apically, with concomitant increase in chemotactic factor expression recruiting neutrophils. These immune cells play an important role in maintaining homeostasis and the protective state in periodontal tissue because they eliminate unwanted bacteria over time. Previous studies indicate a mechanism for attracting immune cells to periodontal tissue with the purpose of maintaining a protective state; although this mechanism can function without bacteria, it is enhanced by the normal flora. A better understanding of the relationship between the protective state and its disruption in periodontal disease could lead to the development of new treatment strategies for periodontal disease.

中文翻译:

维持人体牙周组织的保护状态

由牙周病原体感染引起的牙周炎的主要特征是炎症性骨吸收和结缔组织破坏。简单地将牙周炎描述为一种特定的细菌感染并不能完全解释所观察到的各种牙周组织破坏模式。牙周组织损伤被认为是由多种因素引起的。近年来,牙周病原体的研究目标已经从寻找特定病原体转变为研究损害牙周组织的机制。细菌以几种方式直接与宿主相互作用,影响逃避宿主防御的分子的表达和活性,破坏局部组织并抑制其修复。主人' 先天和后天的免疫系统是重要的防御机制,可保护牙周组织免受牙周病原体的侵袭和侵袭,从而防止感染。先天免疫和后天免疫已发展为应对微生物挑战,在牙周组织中形成了无缝防御网络。在先天免疫反应中,宿主细胞通过专门的受体快速检测细菌细胞壁上存在的大分子和核酸,从而触发保护性炎症反应。宿主免疫子系统的工作主要由吞噬细胞,β-防御素和补体系统完成。此外,口服先天免疫的第一道防线是连接上皮,它是阻止口腔细菌和其他非自身物质进入的物理屏障。在正常菌群的存在下,连接上皮细胞活跃地分化并顶端增殖,伴随着募集嗜中性粒细胞的趋化因子表达的增加。这些免疫细胞在维持牙周组织的稳态和保护状态方面起着重要作用,因为它们会随着时间的流逝消除有害细菌。先前的研究表明了一种以保持保护状态为目的将免疫细胞吸引至牙周组织的机制。尽管这种机制可以在没有细菌的情况下发挥作用,但正常菌群会增强这种机制。对牙周疾病保护状态与其破坏之间关系的更好理解可能会导致牙周疾病新治疗策略的发展。结膜上皮细胞活跃地分化并顶端增殖,伴随着趋化因子表达的募集中性粒细胞的增加。这些免疫细胞在维持牙周组织的稳态和保护状态方面起着重要作用,因为它们会随着时间的流逝消除有害细菌。先前的研究表明了一种以保持保护状态为目的将免疫细胞吸引至牙周组织的机制。尽管这种机制可以在没有细菌的情况下发挥作用,但正常菌群会增强这种机制。对牙周疾病保护状态与其破坏之间关系的更好理解可能会导致牙周疾病新治疗策略的发展。结膜上皮细胞活跃地分化并顶端增殖,伴随着趋化因子表达的募集中性粒细胞的增加。这些免疫细胞在维持牙周组织的稳态和保护状态方面起着重要作用,因为它们会随着时间的流逝消除有害细菌。先前的研究表明了一种以保持保护状态为目的将免疫细胞吸引至牙周组织的机制。尽管这种机制可以在没有细菌的情况下发挥作用,但正常菌群会增强这种机制。对牙周疾病保护状态与其破坏之间关系的更好理解可能会导致牙周疾病新治疗策略的发展。这些免疫细胞在维持牙周组织的稳态和保护状态方面起着重要作用,因为它们会随着时间的流逝消除有害细菌。先前的研究表明了一种以保持保护状态为目的将免疫细胞吸引至牙周组织的机制。尽管这种机制可以在没有细菌的情况下发挥作用,但正常菌群会增强这种机制。对牙周疾病保护状态与其破坏之间关系的更好理解可能会导致牙周疾病新治疗策略的发展。这些免疫细胞在维持牙周组织的稳态和保护状态方面起着重要作用,因为它们会随着时间的流逝消除有害细菌。先前的研究表明了一种以保持保护状态为目的将免疫细胞吸引至牙周组织的机制。尽管这种机制可以在没有细菌的情况下发挥作用,但正常菌群会增强这种机制。对牙周疾病保护状态与其破坏之间关系的更好理解可能会导致牙周疾病新治疗策略的发展。先前的研究表明了一种以保持保护状态为目的将免疫细胞吸引至牙周组织的机制。尽管这种机制可以在没有细菌的情况下发挥作用,但正常菌群会增强这种机制。对牙周疾病保护状态与其破坏之间关系的更好理解可能会导致牙周疾病新治疗策略的发展。先前的研究表明了一种以保持保护状态为目的将免疫细胞吸引至牙周组织的机制。尽管这种机制可以在没有细菌的情况下发挥作用,但正常菌群会增强这种机制。对牙周疾病保护状态与其破坏之间关系的更好理解可能会导致牙周疾病新治疗策略的发展。
更新日期:2021-04-22
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