Revisiting the Page & Schroeder model: the good, the bad and the unknowns in the periodontal host response 40 years later.

Revisiting the Page & Schroeder model: the good, the bad and the unknowns in the periodontal host response 40 years later.
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重新审视佩奇和施罗德模型:40 年后牙周宿主反应的好、坏和未知。

DOI:
10.1111/prd.12181
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发表时间:
2017-10
影响因子:
18.6
通讯作者:
Korostoff JM
Korostoff JM
中科院分区:
医学1区
文献类型:
--
作者:
Hajishengallis G;Korostoff JM

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在1976年的经典论文中,Page和Schroeder描述了炎症性牙周病的组织病理学事件以及参与炎症性牙周病发生和发展的骨髓细胞和淋巴细胞的类型。牙周病发病机制的分期为“初始”,“早期”,“建立”和“先进”的病变,有效地指导了该领域的后续研究,并保持基本有效。然而,关于免疫和炎症反应的诱导,调节和效应器功能的细胞和分子机制的重大进展需要重新评估他们的工作及其与新兴概念的整合。我们现在知道,每种类型的白细胞实际上由功能不同的子集代表,在免疫和炎症中具有不同甚至相互冲突的作用。出乎意料的是,中性粒细胞,传统上被认为只是在急性条件下的抗微生物效应和“初始”病变的主角,目前赞赏其功能的多功能性和在慢性炎症中的关键作用。此外,一个全新的研究领域,骨免疫学,已经发展并阐明了免疫炎症事件对骨骼系统的影响。这些发展和先天性和适应性白细胞之间的串扰相互作用的分子解剖,以及免疫系统和局部稳态机制之间,提供了一个更细致入微的了解牙周炎的主机响应具有深远的意义治疗。与此同时,更深刻的见解产生了新的问题,其中许多问题仍然没有答案。在这篇综述中,Page和Schroeder提出他们的模型后的40年,我们总结了牙周病发病机制的持久和新兴进展。
In their classic 1976 paper, Page & Schroeder described the histopathologic events and the types of myeloid cells and lymphocytes involved in the initiation and progression of inflammatory periodontal disease. The staging of periodontal disease pathogenesis as ‘initial’, ‘early’, ‘established’ and ‘advanced’ lesions, productively guided subsequent research in the field and remains fundamentally valid. However, major advances regarding the cellular and molecular mechanisms underlying the induction, regulation, and effector functions of immune and inflammatory responses necessitate a reassessment of their work and its integration with emerging new concepts. We now know that each type of leukocyte is actually represented by functionally distinct subsets with different or even conflicting roles in immunity and inflammation. Unexpectedly, neutrophils, traditionally regarded as merely anti-microbial effectors in acute conditions and protagonists of the ‘initial’ lesion, are currently appreciated for their functional versatility and critical roles in chronic inflammation. Moreover, an entirely new field of study, osteoimmunology, has developed and shed light on the impact of immunoinflammatory events on the skeletal system. These developments and the molecular dissection of crosstalk interactions between innate and adaptive leukocytes, as well as between the immune system and local homeostatic mechanisms, offer a more nuanced understanding of the host response in periodontitis with profound implications for treatment. At the same time, deeper insights have generated new questions many of which remain unanswered. In this review, forty years after Page & Schroeder proposed their model, we summarize enduring and emerging advances in periodontal disease pathogenesis.
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