在牙周炎中，骨形成和吸收之间的平衡倾向于骨质流失。牙周韧带相关蛋白-1（PLAP-1）和硬化蛋白在抑制骨形成方面起着重要作用。肿瘤坏死因子-α（TNF-α）是与牙周骨质流失有关的中心促炎细胞因子。本研究旨在评估牙周疾病患者龈沟液（GCF）中PLAP-1、硬化蛋白和TNF-α水平。 研究纳入了71位被诊断为广泛III级C期牙周炎（n = 23）、牙龈炎（n = 24）和牙周健康（n = 24）的个体。进行了全口临床牙周测量。通过酶联免疫吸附法量化GCF中的PLAP-1、硬化蛋白和TNF-α总量。使用非参数方法进行数据分析。 牙周炎组的GCF PLAP-1、硬化蛋白和TNF-α水平显著高于牙龈炎和牙周健康组（p<0.05）。牙龈炎组的GCF PLAP-1和TNF-α水平高于健康对照组（p<0.05），而GCF硬化蛋白水平两组相似（p>0.05）。发现GCF PLAP-1、硬化蛋白和TNF-α水平与所有临床参数呈显著正相关（p<0.01）。 据我们所知，这是第一项显示牙周健康和疾病中GCF PLAP-1水平的研究。牙周炎中增加的GCF PLAP-1和硬化蛋白水平及其与TNF-α的相关性意味着这些分子可能参与发病机制。需要进一步在更大的混合队列进行研究，以阐明PLAP-1和硬化蛋白在牙周骨质流失中的可能作用。本文受版权保护。保留所有权利。

In periodontitis, the equilibrium between bone formation and resorption skews in favor of bone loss. Periodontal ligament-associated protein-1 (PLAP-1) and sclerostin play a significant role in the suppression of bone formation. Tumor necrosis factor-alpha (TNF-α) is a central pro-inflammatory cytokine related to periodontal bone loss. This study aims to assess gingival crevicular fluid (GCF) PLAP-1, sclerostin and TNF-α levels in individuals with periodontal disease.Seventy-one individuals diagnosed with generalized stage III grade C periodontitis (n = 23), gingivitis (n = 24) and periodontal health (n = 24) were included in the study. Full-mouth clinical periodontal measurements were performed. PLAP-1, sclerostin and TNF-α total amounts in GCF were quantified by ELISA. Non-parametric methods were used for the data analyses.Periodontitis group exhibited significantly higher GCF PLAP-1, sclerostin and TNF-α levels compared to gingivitis and periodontally healthy groups (p<0.05). GCF PLAP-1 and TNF-α levels of gingivitis group were higher than healthy controls (p<0.05) whereas GCF sclerostin levels were similar in two groups (p>0.05). Significant positive correlations were found between GCF PLAP-1, sclerostin and TNF-α levels and all clinical parameters (p<0.01).To our knowledge, this is the first study showing GCF PLAP-1 levels in periodontal health and disease. Increased GCF PLAP-1 and sclerostin levels and their correlations with TNF-α in periodontitis imply that those molecules might be involved in the pathogenesis of periodontal disease. Further studies in larger mixed cohorts are needed to enlighten the possible role of PLAP-1 and sclerostin in periodontal bone loss. This article is protected by copyright. All rights reserved.This article is protected by copyright. All rights reserved.