Historical and contemporary hypotheses on the development of oral diseases: are we there yet?

Historical and contemporary hypotheses on the development of oral diseases: are we there yet?
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关于口腔疾病发展的历史和当代假设:我们还在吗?

DOI:
10.3389/fcimb.2014.00092
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发表时间:
2014
影响因子:
5.7
通讯作者:
Krom BP
Krom BP
中科院分区:
医学2区
文献类型:
--
作者:
Rosier BT;De Jager M;Zaura E;Krom BP

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牙菌斑是一种口腔生物膜,就像我们的微生物组的其他部分一样,在健康和疾病中发挥作用。具体来说,它是龋齿、牙龈炎和牙周炎等非常常见的口腔疾病的原因。关于口腔疾病发展的想法随着时间的推移而演变。在世纪,由于缺乏技术,科学家无法识别与疾病有关的细菌。这导致了“非特异性菌斑假说”或认为牙菌斑的积累是口腔疾病的原因,而不区分细菌的毒力水平。在20世纪,这一思想随着分析从健康到疾病的变化的技术而发展。第一个常见的假说是“特异性菌斑假说”(1976年),提出只有少数几种微生物菌群与疾病密切相关。其次,更新了“非特异性菌斑假说”(1986年),并通过考虑细菌之间毒力的差异丰富了总微生物群落的整体活性可能导致疾病的观点。然后,考虑了一个假设,该假设结合了前两个假设的关键概念:“生态菌斑假设”(1994年),该假设提出疾病是由于生态压力导致某些疾病相关微生物富集而导致微生物区系失衡的结果。最后,最近的“Keystone-病原体假说”(2012年)提出,某些低丰度的微生物病原体可以通过干扰宿主免疫系统和重塑微生物群而引起炎症性疾病。在这篇全面的综述中,我们描述了这些不同的假设以及围绕它们的想法是如何产生的,并测试了它们目前对理解口腔疾病发展的适用性。最后,我们得出结论,一个包罗万象的生态假说解释从健康到疾病的转变仍然缺乏。
Dental plaque is an oral biofilm that much like the rest of our microbiome has a role in health and disease. Specifically, it is the cause of very common oral diseases such as caries, gingivitis, and periodontitis. The ideas about oral disease development have evolved over time. In the nineteenth century, scientists could not identify bacteria related to disease due to the lack of technology. This led to the “Non-Specific Plaque Hypothesis” or the idea that the accumulation of dental plaque was responsible for oral disease without discriminating between the levels of virulence of bacteria. In the twentieth century this idea evolved with the techniques to analyze the changes from health to disease. The first common hypothesis was the “Specific Plaque Hypothesis” (1976) proposing that only a few species of the total microflora are actively involved in disease. Secondly, the “Non-Specific Plaque Hypothesis” was updated (1986) and the idea that the overall activity of the total microflora could lead to disease, was enriched by taking into account difference in virulence among bacteria. Then, a hypothesis was considered that combines key concepts of the earlier two hypotheses: the “Ecological Plaque Hypothesis” (1994), which proposes that disease is the result of an imbalance in the microflora by ecological stress resulting in an enrichment of certain disease-related micro-organisms. Finally, the recent “Keystone-Pathogen Hypothesis” (2012) proposes that certain low-abundance microbial pathogens can cause inflammatory disease by interfering with the host immune system and remodeling the microbiota. In this comprehensive review, we describe how these different hypotheses, and the ideas around them, arose and test their current applicability to the understanding of the development of oral disease. Finally, we conclude that an all-encompassing ecological hypothesis explaining the shifts from health to disease is still lacking.
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