The Forsyth Institute, Cambridge, Massachusetts, USA.
Medipol University, Faculty of Dentistry, Department of Periodontology, Istanbul, Turkey.
J Periodontol. 2023 Dec;94(12):1425-1435. doi: 10.1002/JPER.23-0274. Epub 2023 Jul 11.
Parkinson's disease (PA) affects 1% of the global population above 60 years. PA pathogenesis involves severe neuroinflammation that impacts systemic and local inflammatory changes. We tested the hypothesis that PA is associated with periodontal tissue inflammation promoting a greater systemic inflammatory burden.
We recruited 60 patients with Stage III, Grade B periodontitis (P) with and without PA (n = 20 for each). We also included systemically and periodontally healthy individuals as controls (n = 20). Clinical periodontal parameters were recorded. Serum, saliva, and gingival crevicular fluid (GCF) samples were collected to measure the inflammatory and neurodegenerative targets (YKL-40, fractalkine, S100B, alpha-synuclein, tau, vascular cell adhesion protein-1 (VCAM-1), brain-derived neurotrophic factor (BDNF), neurofilament light chain (NfL).
Parkinson's patients in this study had mild to moderate motor dysfunctions, which did not prevent them from performing optimal oral hygiene control. Periodontal parameters and GCF volume were significantly higher in the P and P+PA groups than in the control group. PA was associated with significantly increased bleeding on probing (BOP) compared to P-alone (p < 0.05), while other clinical parameters were similar between P and P+PA groups. In saliva and serum, YKL-40 levels were higher in the P+PA group than in P and C groups (p < 0.001). GCF NfL levels from shallow sites were significantly higher in the P+PA group compared to the C group (p = 0.0462). GCF S100B levels from deep sites were higher in the P+PA group than in healthy individuals (p = 0.0194).
The data suggested that PA is highly associated with increased periodontal inflammatory burden-bleeding upon probing and inflammatory markers-in parallel with PA-related neuroinflammation.
帕金森病（PA）影响全球 60 岁以上人群的 1%。PA 的发病机制涉及严重的神经炎症，影响全身和局部炎症变化。我们检验了这样一个假设，即 PA 与牙周组织炎症有关，从而导致更大的全身炎症负担。
我们招募了 60 名患有 III 期 B 级牙周炎（P）的患者，其中有和没有 PA（每组 20 名）。我们还纳入了系统和牙周健康的个体作为对照组（每组 20 名）。记录临床牙周参数。采集血清、唾液和龈沟液（GCF）样本，以测量炎症和神经退行性变指标（YKL-40、 fractalkine、S100B、α-突触核蛋白、tau、血管细胞黏附蛋白-1（VCAM-1）、脑源性神经营养因子（BDNF）、神经丝轻链（NfL）。
本研究中的帕金森病患者有轻到中度运动功能障碍，但这并未妨碍他们进行最佳的口腔卫生控制。与对照组相比，P 组和 P+PA 组的牙周参数和 GCF 体积明显更高。与 P 组相比，PA 组的探诊出血（BOP）显著增加（p<0.05），而 P 组和 P+PA 组的其他临床参数相似。在唾液和血清中，P+PA 组的 YKL-40 水平高于 P 组和 C 组（p<0.001）。与 C 组相比，P+PA 组的浅牙周袋 GCF NfL 水平显著升高（p=0.0462）。与健康个体相比，P+PA 组的深牙周袋 GCF S100B 水平更高（p=0.0194）。
数据表明，PA 与牙周炎症负担增加密切相关，表现为探诊出血和炎症标志物增加，与 PA 相关的神经炎症平行。
