多囊卵巢综合征妇女中的牙龈炎与白细胞-内皮细胞相互作用

考虑到慢性炎症与牙周疾病及心血管风险增加之间的关联，本研究旨在探讨牙龈炎是否会加剧多囊卵巢综合征（PCOS）妇女的炎症反应及亚临床动脉粥样硬化标志物。为此采用病例对照研究，将妇女分为三组：两组为PCOS（有和无牙龈炎）及一对照组。测定人体测量学和生化指标，以及牙周参数（探诊袋深度[PPD]、临床附着水平[CAL]、探诊出血[BOP]、菌斑指数、结石指数和牙齿缺失）、系统性及中性粒细胞炎症标志物（肿瘤坏死因子α[TNFα]、C反应蛋白[CRP]和c-Jun N末端激酶[JNK]）、系统性氧化应激介质（髓过氧化物酶[MPO]和谷胱甘肽）、可溶性细胞粘附分子及中性粒细胞-内皮细胞相互作用（滚动通量、速度和粘附）。共招募104名女性，其中68例患PCOS，24例伴牙龈炎，36例为对照组。PCOS患者表现出性激素、脂质及碳水化合物指标异常。系统性炎症标志物、MPO及可溶性血小板选择素[sP-selectin]水平升高，谷胱甘肽水平降低。伴牙龈炎的PCOS患者其BOP、菌斑及结石指数更高。中性粒细胞在PCOS伴牙龈炎组中表现出JNK升高和粘附能力降低，伴随流动条件下滚动速度减慢、滚动通量增加及细胞粘附增强，这些变化在有牙龈炎的患者中更为明显。BOP与滚动速度、滚动通量及细胞粘附独立相关。伴牙龈炎的PCOS患者的中性粒细胞表现出超常活性，更易与内皮细胞相互作用，可能促进动脉粥样硬化的发生。当前，牙周疾病在成人中具有高发率，影响口腔健康及生活质量，导致牙齿移动、咀嚼功能障碍甚至牙齿丧失。近年来，牙周医学的概念逐渐兴起，研究牙周疾病如何影响全身炎症反应及系统性炎症疾病对口腔健康的影响。本研究评估了患有多囊卵巢综合征的女性，发现其牙龈炎患病率较高，且影响白细胞与内皮细胞的相互作用。这些女性的中性粒细胞表现出超常反应，粘附性增强、流动速度降低、滚动增强。这一研究为分析牙龈炎患者中性粒细胞的超活性提供了新的研究方向，揭示其在动脉粥样硬化中的潜在作用机制。

Given the link between chronic inflammation and periodontal pathologies and increased cardiovascular risk, this study aims to investigate if gingivitis exacerbates the inflammatory response and subclinical atherosclerotic markers in women with polycystic ovary syndrome (PCOS).For this case-control study, women were assigned to three groups: two PCOS groups (with and without gingivitis) and a control group. Anthropometric and biochemical variables were determined, along with periodontal parameters (probing pocket depth [PPD], clinical attachment level [CAL], bleeding on probing [BOP], plaque index, calculus index, and tooth loss), systemic and neutrophil inflammatory markers (tumor necrosis factor alpha [TNFα], C-reactive protein [CRP], and c-Jun N-terminal kinase [JNK]), systemic oxidative stress mediators (myeloperoxidase [MPO] and glutathione), soluble cellular adhesion molecules, and neutrophil-endothelium cell interactions (rolling flux, velocity, and adhesion).Of 104 women recruited, 68 had PCOS, 24 of whom presented gingivitis, and 36 were controls. PCOS patients presented altered sexual hormone, lipid, and carbohydrate profiles. Levels of systemic inflammatory markers, MPO, and soluble platelet selectin (sP-selectin) were higher, and glutathione levels were lower in PCOS patients. BOP, plaque, and calculus index values were higher in PCOS patients with gingivitis. Neutrophils from PCOS patients showed increased JNK and decreased adhesion under flow conditions, with reduced rolling velocity and increased rolling flux and cellular adhesion, all of which were more pronounced in those with gingivitis. BOP was independently associated with rolling velocity, rolling flux, and cellular adhesion.Neutrophils of PCOS patients with gingivitis exhibit hyperactivity, promoting interaction with the endothelium and potentially contributing to atherosclerotic disease.Currently, there is a high prevalence of diseases that affect tooth-supporting tissues (periodontal diseases) and negatively influence the oral health and quality of life of the adult population. These pathologies lead to movement of the teeth and impairment of chewing function, eventually resulting in the loss of teeth. In recent years, the concept of periodontal medicine has arisen and consists of studying how periodontal diseases can influence our general inflammatory system and how systemic inflammatory pathologies can affect our oral health. In the present study, we evaluate a group of women with polycystic ovary syndrome (PCOS), a condition characterized by alterations of sex hormones and lipid profile and weight gain (body mass index). Our results show a high prevalence of gum inflammation among women with PCOS, which affects the interaction of their leukocytes and endothelial cells. The leukocytes of these women are hyper-responsive, presenting greater endothelial adhesion, lower flow velocity and enhanced rolling compared to those in a PCOS group without gum inflammation or controls. This study has generated a new line of research to analyze how neutrophils from patients with gingivitis exhibit hyperactivity, which promotes their interaction with the endothelium, thus contributing to the development of atherosclerotic disease.