AimTo investigate the hypothesis supporting the link between periodontitis and dopaminergic neuron degeneration.Materials and MethodsAdult male Wistar rats were used to induce dopaminergic neuronal injury with 6‐hydroxydopamine (6‐OHDA) neurotoxin and experimental periodontitis via ligature placement. Motor function assessments were conducted before and after periodontitis induction in controls and 6‐OHDA‐injury‐induced rats. Tissue samples from the striatum, jaw and blood were collected for molecular analyses, encompassing immunohistochemistry of tyrosine hydroxylase, microglia and astrocyte, as well as micro‐computed tomography, to assess alveolar bone loss and for the analysis of striatal oxidative stress and plasma inflammatory markers.ResultsThe results indicated motor impairment in 6‐OHDA‐injury‐induced rats exacerbated by periodontitis, worsening dopaminergic striatal degeneration. Periodontitis alone or in combination with 6‐OHDA‐induced lesion was able to increase striatal microglia, while astrocytes were increased by the combination only. Periodontitis increased striatal reactive oxygen species levels and plasma tumour necrosis factor‐alpha levels in rats with 6‐OHDA‐induced lesions and decreased the anti‐inflammatory interleukin‐10.ConclusionsThis study provides original insights into the association between periodontitis and a neurodegenerative condition. The increased inflammatory pathway associated with both 6‐OHDA‐induced dopaminergic neuron lesion and periodontal inflammatory processes corroborates that the periodontitis‐induced systemic inflammation may aggravate neuroinflammation in Parkinson's‐like disease, potentially hastening disease progression.

中文翻译：

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实验性牙周炎加剧多巴胺能神经元变性


目的探讨支持牙周炎与多巴胺能神经元变性之间联系的假说。材料与方法成年雄性Wistar大鼠通过6-羟基多巴胺（6-OHDA）神经毒素诱导多巴胺能神经元损伤，并通过结扎法诱导实验性牙周炎。在对照组和 6-OHDA 损伤诱导的大鼠牙周炎诱导之前和之后进行运动功能评估。收集纹状体、颌骨和血液的组织样本进行分子分析，包括酪氨酸羟化酶、小胶质细胞和星形胶质细胞的免疫组织化学以及微型计算机断层扫描，以评估牙槽骨丢失并分析纹状体氧化应激和血浆炎症标志物结果结果表明，6-OHDA 损伤引起的大鼠的运动障碍因牙周炎而加剧，多巴胺能纹状体变性恶化。单独的牙周炎或与 6-OHDA 诱导的病变相结合能够增加纹状体小胶质细胞，而星形胶质细胞仅通过组合而增加。牙周炎增加了 6-OHDA 诱导病变大鼠纹状体活性氧水平和血浆肿瘤坏死因子-α 水平，并降低了抗炎白细胞介素-10。结论本研究为牙周炎与神经退行性疾病之间的关联提供了原始见解。与 6-OHDA 诱导的多巴胺能神经元病变和牙周炎症过程相关的炎症途径增加证实，牙周炎诱导的全身炎症可能会加重帕金森病样疾病的神经炎症，可能加速疾病进展。