Liukkonen A, He Q, Gürsoy U K, Pussinen P J, Gröndahl-Yli-Hannuksela K, Liukkonen J, Sorsa T, Suominen A L, Huumonen S, Könönen E
Institute of Dentistry, University of Turku, Turku, Finland.
Department of Medical Microbiology and Immunology, University of Turku, Turku, Finland.
J Periodontal Res. 2017 Jun;52(3):540-545. doi: 10.1111/jre.12420. Epub 2016 Sep 14.
Mannose-binding lectin (MBL) plays an important role in innate immunity. MBL deficiency is usually caused by mutations in exon 1 of the MBL structural gene (MBL2). Our aim was to investigate MBL2 polymorphisms and their relation to salivary levels of periodontal inflammatory/tissue destruction markers and two major periodontitis-associated bacteria.
Salivary samples from 222 subjects were available for genotyping by pyrosequencing. The subjects between 40 and 60 years of age and having a minimum of 20 teeth were divided into three periodontal groups: 80 had generalized periodontitis, 65 had localized periodontitis and 77 were periodontitis-free. A comparison between their MBL2 genotypes and salivary detection rates and levels of Aggregatibacter actinomycetemcomitans and Porphyromonas gingivalis as well as interleukin -1β, matrix metalloproteinase -8, and tissue inhibitor of matrix metalloproteinase (TIMP)-1 was performed.
The frequencies of the MBL2 wild-type (A/A), heterozygote variants (A/O) and homozygote variants (O/O) were 69.4%, 26.6% and 4%, respectively. In A. actinomycetemcomitans-positive subjects having homozygote or heterozygote MBL2 variants, the salivary concentrations of IL-1β (p = 0.010) were elevated and those of TIMP-1 (p = 0.001) were decreased. In addition their matrix metalloproteinase -8/TIMP-1 ratio was higher (p < 0.001) and they had more pocket teeth (p = 0.012) than subjects negative for A. actinomycetemcomitans.
Our findings indicate that the carriage of A. actinomycetemcomitans may facilitate extended periodontal inflammation and destruction in subjects with a variant form of human MBL2.
甘露糖结合凝集素（MBL）在固有免疫中发挥重要作用。MBL缺乏通常由MBL结构基因（MBL2）外显子1的突变引起。我们的目的是研究MBL2多态性及其与牙周炎症/组织破坏标志物唾液水平以及两种主要的牙周炎相关细菌的关系。
222名受试者的唾液样本可用于焦磷酸测序基因分型。年龄在40至60岁之间且至少有20颗牙齿的受试者被分为三个牙周组：80人患有广泛性牙周炎，65人患有局限性牙周炎，77人无牙周炎。对他们的MBL2基因型与牙龈卟啉单胞菌和伴放线放线杆菌的唾液检测率及水平以及白细胞介素-1β、基质金属蛋白酶-8和基质金属蛋白酶组织抑制剂（TIMP）-1进行了比较。
MBL2野生型（A/A）、杂合子变体（A/O）和纯合子变体（O/O）的频率分别为69.4%、26.6%和4%。在伴有MBL2纯合子或杂合子变体的伴放线放线杆菌阳性受试者中，白细胞介素-1β的唾液浓度升高（p = 0.010），TIMP-1的唾液浓度降低（p = 0.001）。此外，与伴放线放线杆菌阴性的受试者相比，他们的基质金属蛋白酶-8/TIMP-1比值更高（p < 0.001），且牙周袋牙更多（p = 0.012）。
我们的研究结果表明，伴放线放线杆菌的携带可能会促进人类MBL2变异形式受试者的牙周炎症扩展和组织破坏。
