Komiyama Yuske, Kafkova Leona Raskova, Barasch Andrei, Shah Ging R, Grbic John T, Novak Zdenek, Komiyama Kazuo, Novak Jan, Mestecky Jiri, Moldoveanu Zina
Department of Microbiology, University of Alabama at Birmingham, Birmingham, AL.
J Periodontol. 2014 Dec;85(12):1779-85. doi: 10.1902/jop.2014.140212.
Periodontitis is a chronic inflammatory disease initiated by a synergistic and dysbiotic microbial community that elicits a gingival inflammatory response leading to tissue breakdown. Periodontitis shares many characteristics with other chronic inflammatory diseases, including abnormal glycosylation of immunoglobulin (Ig)G. The current authors have previously demonstrated that IgG from gingival crevicular fluid (GCF) of patients with chronic periodontitis contains galactose (Gal)-deficient IgG.
The origin of the aberrantly glycosylated IgG was determined by measuring levels of Gal-deficient IgG in GCF and serum from patients with periodontitis and non-periodontitis controls using lectin enzyme-linked immunosorbent assay. The Ig-producing cells and the proportion of cells producing Gal-deficient IgG were immunohistochemically determined in gingival tissues from patients with periodontitis by fluorescence microscopy. The results were statistically evaluated and correlated with clinical data.
The results indicate that GCF of patients with periodontitis had higher levels of Gal-deficient IgG compared with controls (P = 0.002). In gingival tissues, IgG was the dominant isotype among Ig-producing cells, and 60% of IgG-positive cells produced Gal-deficient IgG. Moreover, the proportion of Gal-deficient IgG-producing cells directly correlated with clinical parameters of probing depth and clinical attachment loss (AL).
These results suggest that the presence of Gal-deficient IgG is associated with gingival inflammation and may play a role in the worsening of clinical parameters of periodontitis, such as AL.
牙周炎是一种由协同失调的微生物群落引发的慢性炎症性疾病，会引发牙龈炎症反应，导致组织破坏。牙周炎与其他慢性炎症性疾病有许多共同特征，包括免疫球蛋白（Ig）G糖基化异常。本文作者此前已证明，慢性牙周炎患者龈沟液（GCF）中的IgG含有半乳糖（Gal）缺陷型IgG。
通过使用凝集素酶联免疫吸附测定法测量牙周炎患者和非牙周炎对照者的GCF和血清中Gal缺陷型IgG的水平，确定异常糖基化IgG的来源。通过荧光显微镜免疫组织化学法测定牙周炎患者牙龈组织中产生Ig的细胞以及产生Gal缺陷型IgG的细胞比例。对结果进行统计学评估，并与临床数据相关联。
结果表明，与对照组相比，牙周炎患者的GCF中Gal缺陷型IgG水平更高（P = 0.002）。在牙龈组织中，IgG是产生Ig的细胞中的主要亚型，60%的IgG阳性细胞产生Gal缺陷型IgG。此外，产生Gal缺陷型IgG的细胞比例与探诊深度和临床附着丧失（AL）的临床参数直接相关。
这些结果表明，Gal缺陷型IgG的存在与牙龈炎症相关，可能在牙周炎临床参数（如AL）的恶化中起作用。
