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实验性种植体周围炎引起神经炎症:大鼠的探索性研究。

Experimental peri-implantitis induces neuroinflammation: An exploratory study in rats.

机构信息

Department of Oral Surgery and Implantology, Goethe University, Carolinum, Frankfurt am Main, Germany.

Department of Periodontology, School of Dentistry, Universidad Científica del Sur, Lima, Perú.

出版信息

BMC Oral Health. 2024 Oct 18;24(1):1238. doi: 10.1186/s12903-024-04995-z.

Abstract

PURPOSE

Cumulating evidence supports the close association between periodontal diseases, neuroinflammation and neurodegenerative pathologies, except for peri-implantitis (PI). Thus, this study explored the association between experimental PI and neuropathological changes in the rat brain.

MATERIALS AND METHODS

After bilateral first molars extraction, experimental PI was induced at titanium implants placed in the maxillae by lipopolysaccharide injections and ligature placement. Following 28-weeks of disease progression, the maxillae and brains were retrieved from 6 rats. Healthy brains from 3 rats were used as control. Brains were analyzed by immunohistochemistry to detect signs of neuroinflammation (interleukin (IL)-6 and tumor necrosis factor (TNF)-α)), microglial activation (IBA-1) and astrogliosis (GFAP). To explore signs of neurodegeneration, hematoxylin/eosin and Nissl stainings were used. Also, four different antibodies against amyloid beta (Aβ 1-42) were tested.

RESULTS

Chronic PI lesions showed peri-implant bone resorption accompanied by large inflammatory infiltrates. IL-6 and TNF-α cells were found within the CA1 and Dentate Gyrus regions of the hippocampus of the PI-affected group, while almost no immune-positivity was detected in the control (p < 0.05). Detection of activated GFAP microglia and IBA-1 astrocytes surface were significantly higher at the CA areas, and cerebral cortex of the PI-affected group, in comparison with control (p < 0.05). Shrunk neurons with pyknotic nuclei were inconsistently found among the PI-affected group, and these were almost not detected in control. No positive Aβ reactivity was detected in any of the samples.

CONCLUSION

Chronic experimental PI lesions led to an increased detection of IL-6 and TNF-α, GFAP microgliosis and IBA-1 astrocytosis, and in some cases, neurodegeneration, in the rat brain.

摘要

目的

越来越多的证据支持牙周病、神经炎症和神经退行性病变之间的密切关联,但不包括种植体周围炎(PI)。因此,本研究探讨了实验性 PI 与大鼠大脑神经病理学变化之间的关系。

材料和方法

在双侧第一磨牙拔除后,通过在钛植入物上注射脂多糖和结扎放置,在上颌诱导实验性 PI。在疾病进展 28 周后,从 6 只大鼠中取出上颌骨和大脑。从 3 只健康大鼠中取出健康大脑作为对照。通过免疫组织化学检测检测神经炎症(白细胞介素(IL)-6 和肿瘤坏死因子(TNF)-α)、小胶质细胞激活(IBA-1)和星形胶质细胞增生(GFAP)的迹象。为了探索神经退行性变的迹象,使用苏木精/伊红和尼氏染色。还测试了四种不同的淀粉样蛋白β(Aβ 1-42)抗体。

结果

慢性 PI 病变表现为种植体周围骨吸收伴大量炎症浸润。在 PI 病变组的海马 CA1 和齿状回区发现了 IL-6 和 TNF-α 细胞,而在对照组几乎没有免疫阳性细胞(p<0.05)。在 PI 病变组的 CA 区和大脑皮层,活化的 GFAP 小胶质细胞和 IBA-1 星形胶质细胞表面的检测明显高于对照组(p<0.05)。PI 病变组中发现了核固缩的缩小神经元,但在对照组中几乎未检测到。在任何样本中均未检测到阳性 Aβ 反应性。

结论

慢性实验性 PI 病变导致大鼠大脑中 IL-6 和 TNF-α、GFAP 小胶质细胞增生和 IBA-1 星形胶质细胞增生的检测增加,在某些情况下还导致神经退行性变。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4bcd/11490110/c8a31cca285f/12903_2024_4995_Fig1_HTML.jpg

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