降低了GCF DEL-1和增加了GCF中性粒细胞,随着探测口袋深度的增加
Seong-Ho Jin1, Eun-Mi Lee2, Jun-Beom Park1,2
1Department of Dentistry, Graduate School, The Catholic University of Korea, Seoul, Korea.
Journal of periodontal & implant science
|September 8, 2023
概括
在牙裂液 (GCF) 中的发育性内皮位-1 (DEL-1) 与牙周炎患者的探针口袋深度有负相关性,这表明具有保护作用. 唾液DEL-1水平与炎症标志物相关,但不是临床参数.
科学领域:
- 牙周病研究 牙周病研究
- 免疫学和炎症的研究
背景情况:
- 发育性内皮位-1 (DEL-1) 涉及到中性粒细胞在周期内迁移.
- 了解DEL-1在牙周炎病原体中的作用对于开发向疗法至关重要.
研究的目的:
- 在牙周炎患者的唾液和牙裂液 (GCF) 中评估DEL-1的水平.
- 评估DEL-1水平,中性粒细胞计数和临床牙周指标之间的相关性.
主要方法:
- 在40名牙周炎患者中评估了临床牙周指标.
- 在唾液和GCF中测量了DEL-1,IL-1β,IL-6和IL-8的水平.
- 中性粒细胞计数在口服冲洗和GCF样本中确定;使用了斯皮尔曼相关性.
主要成果:
- GCF中的DEL-1水平与探测口袋深度 (PPD) 有负相关性.
- 口腔冲洗和GCF中的中性粒细胞与PPD,IL-8和IL-1β正相关.
- 唾液DEL-1与IL-8和IL-1β相关,但与临床牙周炎参数无关.
结论:
- GCF DEL-1和PPD之间的反向关系支持DEL-1在牙周炎中的潜在保护功能.
- 需要进一步的研究来阐明DEL-1在牙周健康和疾病中的确切机制.
相关概念视频
Peptic Ulcer Disease II: Pathophysiology
Peptic Ulcer Disease (PUD) is characterized by the development of ulcers in the stomach or duodenal mucosa. Its pathophysiology is complex, involving a balance between damaging and protective elements.
Damaging agents such as Helicobacter pylori, gastric acid, pepsin, and nonsteroidal anti-inflammatory drugs (NSAIDs) can weaken the mucosal defense, allowing hydrogen ions to infiltrate back and harm epithelial cells.
Damaging agents such as Helicobacter pylori, gastric acid, pepsin, and nonsteroidal anti-inflammatory drugs (NSAIDs) can weaken the mucosal defense, allowing hydrogen ions to infiltrate back and harm epithelial cells.
Peptic Ulcer Disease II: Pathophysiology
Peptic ulcer disease develops when protective mechanisms of the gastrointestinal mucosa are overwhelmed by harmful factors, leading to localized erosions in the stomach or proximal duodenum. The main causes are Helicobacter pylori infection and chronic use of nonsteroidal anti-inflammatory drugs (NSAIDs).Helicobacter pylori–Induced InjuryBacterial Adaptation and Colonization:H. pylori is a spiral, Gram-negative bacterium adapted to the acidic stomach. and transmitted through oral-oral or...


