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伴放线放线杆菌诱导的牙周病促进大鼠牙周组织的全身和局部反应。

A.actinomycetemcomitans-induced periodontal disease promotes systemic and local responses in rat periodontium.

机构信息

Department of Prosthodontics and Periodontics, Piracicaba Dental School, University of Campinas, Piracicaba, São Paulo, Brazil.

出版信息

J Clin Periodontol. 2012 Apr;39(4):333-41. doi: 10.1111/j.1600-051X.2011.01847.x. Epub 2012 Feb 7.

DOI:10.1111/j.1600-051X.2011.01847.x
PMID:22313458
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3330439/
Abstract

AIM

To characterize the histologic and cellular response to A. actinomycetemcomitans (Aa) infection.

MATERIAL & METHODS: Wistar rats infected with Aa were evaluated for antibody response, oral Aa colonization, loss of attachment, PMN recruitment, TNF-α in the junctional epithelium and connective tissue, osteoclasts and adaptive immune response in local lymph nodes at baseline and 4, 5 or 6 weeks after infection. Some groups were given antibacterial treatment at 4 weeks.

RESULTS

An antibody response against Aa occurred within 4 weeks of infection, and 78% of inoculated rats had detectable Aa in the oral cavity (p < 0.05). Aa infection significantly increased loss of attachment that was reversed by antibacterial treatment (p < 0.05). TNF-α expression in the junctional epithelium followed the same pattern. Aa stimulated high osteoclast formation and TNF-α expression in the connective tissue (p < 0.05). PMN recruitment significantly increased after Aa infection (p < 0.05). Aa also increased the number of CD8(+) T cells (p < 0.05), but not CD4(+) T cells or regulatory T cells (Tregs) (p > 0.05).

CONCLUSION

Aa infection stimulated a local response that increased numbers of PMNs and TNF-α expression in the junctional epithelium and loss of attachment. Both TNF-α expression in JE and loss of attachment was reversed by antibiotic treatment. Aa infection also increased TNF-α in the connective tissue, osteoclast numbers and CD8(+) T cells in lymph nodes. The results link Aa infection with important characteristics of periodontal destruction.

摘要

目的

描述对伴放线放线杆菌(Aa)感染的组织学和细胞反应特征。

材料与方法

用伴放线放线杆菌感染 Wistar 大鼠,评估抗体应答、口腔伴放线放线杆菌定植、丧失附着、PMN 募集、结合上皮和结缔组织中的 TNF-α、破骨细胞和局部淋巴结中的适应性免疫应答,在感染后 4、5 或 6 周时进行基线评估。部分组在第 4 周时给予抗菌治疗。

结果

感染后 4 周内出现针对 Aa 的抗体应答,78%接种大鼠的口腔可检测到 Aa(p<0.05)。伴放线放线杆菌感染显著增加丧失附着,抗菌治疗可逆转(p<0.05)。结合上皮中的 TNF-α表达也呈现相同模式。伴放线放线杆菌刺激破骨细胞形成和结缔组织中 TNF-α表达增加(p<0.05)。PMN 募集在 Aa 感染后显著增加(p<0.05)。伴放线放线杆菌还增加了 CD8(+)T 细胞的数量(p<0.05),但不增加 CD4(+)T 细胞或调节性 T 细胞(Tregs)(p>0.05)。

结论

伴放线放线杆菌感染刺激局部反应,增加结合上皮中的 PMN 和 TNF-α表达以及丧失附着。结合上皮中的 TNF-α表达和丧失附着均可通过抗生素治疗逆转。伴放线放线杆菌感染还增加了结缔组织中的 TNF-α、破骨细胞数量和淋巴结中的 CD8(+)T 细胞。这些结果将伴放线放线杆菌感染与牙周破坏的重要特征联系起来。

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Aggregatibacter (Actinobacillus) actinomycetemcomitans: a triple A* periodontopathogen?伴放线聚集杆菌(放线杆菌属):一种“三A”型牙周病原体?
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