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

实验性种植体周围炎诱发神经炎症:一项大鼠探索性研究

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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.

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