We previously detected a submicromolar concentration of lysophosphatidic acid (LPA) in human saliva. Here, we compare LPA concentrations in human gingival crevicular fluid (GCF) from patients with periodontitis and healthy controls, and examine how the local LPA levels are regulated enzymatically. The concentrations of LPA and its precursor lysophospholipids in GCF was measured by liquid chromatography-tandem mass spectrometry. The LPA-producing and LPA-degrading enzymatic activities were measured by quantifying the liberated choline and free fatty acid, respectively. The concentration of LPA in GCF of periodontitis patients was lower than that of healthy controls, due to higher soluble lysophospholipase activity toward LPA. LPA was found to prevent survival of Sa3, a human gingival epithelium-derived tumor cell line, activate Sa3 through Ca2+ mobilization, and release interleukin 6 from Sa3 in vitro. Furthermore, local injection of LPA into the gingiva attenuated ligature-induced experimental alveolar bone loss induced by oral bacteria inoculation in a rat model of periodontitis in vivo. A high concentration of LPA in human GCF is necessary to maintain normal gingival epithelial integrity and function, protecting the progression of periodontitis.

中文翻译：

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牙周炎患者的牙龈沟液中的溶血磷脂酸含量低，这归因于其可溶性溶血磷脂酶活性高：其对牙周炎引起的牙槽骨丢失的潜在保护作用。

我们以前检测到人类唾液中亚微摩尔浓度的溶血磷脂酸（LPA）。在这里，我们比较了来自牙周炎患者和健康对照者的人齿龈沟液（GCF）中LPA的浓度，并研究了局部LPA水平如何通过酶调节。通过液相色谱-串联质谱法测量GCF中LPA及其前体溶血磷脂的浓度。通过分别定量释放的胆碱和游离脂肪酸来测量产生LPA和降解LPA的酶活性。由于对LPA的可溶性溶血磷脂酶活性较高，因此牙周炎患者GCF中LPA的浓度低于健康人。发现LPA会阻止Sa3（一种人类牙龈上皮衍生的肿瘤细胞系）的存活，通过Ca2 +动员激活Sa3，并在体外从Sa3中释放白介素6。此外，在体内牙周炎的大鼠模型中，向牙龈局部注射LPA可减轻由口腔细菌接种引起的结扎诱导的实验性牙槽骨丢失。人GCF中高浓度的LPA对于维持正常的牙龈上皮完整性和功能，保护牙周炎的进展是必要的。