Jayakumar Sunandhakumari Vishnu, Sadasivan Arun, Koshi Elizabeth, Krishna Aswathy, Alim Aneesh, Sebastian Aneesh
Department of Periodontics and Oral Implantology, PMS College of Dental Science and Research Centre, Trivandrum-695028, India.
Department of Periodontics and Oral Implantology, Sreemookambika Institute of Dental Science and Research, Tamil Nadu-629161, India.
Dent J (Basel). 2018 Jun 13;6(2):19. doi: 10.3390/dj6020019.
For years the pathogenesis of periodontitis was under an immunological Th1/Th2 paradigm. Th1 cells are considered to afford protection against the intracellular pathogens. These cells produce the interferons (IFN) that are involved in macrophage activation, which, in turn, plays an important role in phagocytosis, complement fixation, and opsonization. Th2 cells are thought to have evolved as a form of protection against parasitic helminthes. Th17 subset of CD4Not Necessary+ T cells was identified in the year 2005, which added greater complexity to Th function and are pro inflammatory in nature. Interleukins (ILs) have the ability to alter immunological changes and they also possess the ability to regulate lymphocyte differentiation and haemopoietic stem cells, cell proliferation, and motility, which are classified as pro-inflammatory and anti-inflammatory. There are numerous studies that reported IL-17 levels associated with chronic periodontitis (CP) development. Type II diabetes mellitus (DM) is considered a risk factor for the development of periodontal diseases because the incidence, progression, and severity of periodontal diseases are more common with Type II DM than without DM. This study was aimed at evaluating whether non-surgical periodontal therapy had any effect on plasma concentrations of Interleukin-17 in systemically healthy chronic periodontitis patients and in chronic periodontitis patients with well controlled Type II Diabetes mellitus. Patients were divided into the two groups including the chronic periodontitis group (20 subjects) and the chronic periodontitis with well-controlled Type II Diabetes mellitus group (20 subjects). The Gingival Index and Plaque Index as well as the clinical Attachment Level (CAL) were taken from all the patients of two groups after evaluating fasting blood sugar, post prandial blood sugar, and the Glycated Hemoglobin Level (HbA1c). Then 5 mL blood samples were collected from each patient and plasma was separated and the IL-17 level is evaluated using the ELISA method. Then, as part of phase I periodontal therapy, scaling and root planning was performed. Patients were recalled after one month and clinical and biochemical parameters were reevaluated. Non-surgical periodontal therapy resulted in a reduction of plasma levels of IL-17 in chronic periodontitis patients with and without well controlled Type II Diabetes mellitus.
多年来,牙周炎的发病机制一直处于免疫 Th1/Th2 范式之下。Th1 细胞被认为可提供针对细胞内病原体的保护。这些细胞产生参与巨噬细胞活化的干扰素(IFN),而巨噬细胞活化在吞噬作用、补体固定和调理作用中起重要作用。Th2 细胞被认为是作为一种针对寄生蠕虫的保护形式而进化而来。2005 年发现了 CD4+ T 细胞的 Th17 亚群,这增加了 Th 功能的复杂性,并且其本质上具有促炎作用。白细胞介素(ILs)有能力改变免疫变化,它们还具有调节淋巴细胞分化、造血干细胞、细胞增殖和运动的能力,这些被分类为促炎和抗炎。有许多研究报道了与慢性牙周炎(CP)发展相关的 IL-17 水平。II 型糖尿病(DM)被认为是牙周疾病发展的一个危险因素,因为与非糖尿病患者相比,II 型糖尿病患者中牙周疾病的发病率、进展和严重程度更为常见。本研究旨在评估非手术牙周治疗对全身健康的慢性牙周炎患者和 II 型糖尿病控制良好的慢性牙周炎患者血浆白细胞介素 -17 浓度是否有任何影响。患者被分为两组,包括慢性牙周炎组(20 名受试者)和 II 型糖尿病控制良好的慢性牙周炎组(20 名受试者)。在评估空腹血糖、餐后血糖和糖化血红蛋白水平(HbA1c)后,从两组所有患者中获取牙龈指数、菌斑指数以及临床附着水平(CAL)。然后从每位患者采集 5 mL 血样,分离血浆,并使用 ELISA 方法评估 IL-17 水平。然后,作为 I 期牙周治疗的一部分,进行龈上洁治和根面平整。一个月后召回患者,重新评估临床和生化参数。非手术牙周治疗导致患有和未患有 II 型糖尿病且病情控制良好的慢性牙周炎患者血浆 IL-17 水平降低。