PDF(Pubmed)
Abstract：
The subgingival biofilm attached to tooth surfaces triggers and maintains periodontitis. Previously, late-onset periodontitis has been considered a consequence of dysbiosis and a resultant polymicrobial disruption of host homeostasis. However, a multitude of studies did not show \"healthy\" oral microbiota pattern, but a high diversity depending on culture, diets, regional differences, age, social state etc. These findings relativise the aetiological role of the dysbiosis in periodontitis. Furthermore, many late-onset periodontitis traits cannot be explained by dysbiosis; e.g. age-relatedness, attenuation by anti-ageing therapy, neutrophil hyper-responsiveness, and microbiota shifting by dysregulated immunity, yet point to the crucial role of dysregulated immunity and neutrophils in particular. Furthermore, patients with neutropenia and neutrophil defects inevitably develop early-onset periodontitis. Intra-gingivally injecting lipopolysaccharide (LPS) alone causes an exaggerated neutrophil response sufficient to precipitate experimental periodontitis. Vice versa to the surplus of LPS, the increased neutrophil responsiveness characteristic for late-onset periodontitis can effectuate gingiva damage likewise. The exaggerated neutrophil extracellular trap (NET) response in late-onset periodontitis is blameable for damage of gingival barrier, its penetration by bacteria and pathogen-associated molecular patterns (PAMPs) as well as stimulation of Th17 cells, resulting in further neutrophil activation. This identifies the dysregulated immunity as the main contributor to periodontal disease.
摘要：
附着在牙齿表面的龈下生物膜引发并维持牙周炎。以前,晚发性牙周炎被认为是菌群失调和由此导致的宿主稳态多微生物破坏的结果。然而,大量研究没有显示“健康”的口腔微生物群模式，但是高度的多样性取决于文化，饮食，地区差异,年龄,社会状态等。这些发现与牙周炎中菌群失调的病因学作用相对应。此外，许多迟发性牙周炎特征不能用菌群失调来解释；例如年龄相关性，抗衰老治疗的衰减，中性粒细胞高反应性，和微生物群通过失调的免疫力而转移，然而，指出失调的免疫和中性粒细胞的关键作用。此外，中性粒细胞减少和中性粒细胞缺陷的患者不可避免地会发生早发性牙周炎.仅向牙龈内注射脂多糖（LPS）会引起过度的中性粒细胞反应，足以引起实验性牙周炎。反之亦然，LPS的盈余，迟发性牙周炎的嗜中性粒细胞反应性增加的特征也可以影响牙龈损伤。晚发性牙周炎中过度的中性粒细胞胞外陷阱（NET）反应应归咎于牙龈屏障的损伤，它通过细菌和病原体相关分子模式（PAMPs）的渗透以及Th17细胞的刺激，导致中性粒细胞进一步活化。这将失调的免疫鉴定为牙周疾病的主要促成因素。
