A1 Journal article – refereed
Mannose-binding lectin gene polymorphism in relation to periodontal infection

List of Authors: Liukkonen A, He Q, Gürsoy UK, Pussinen PJ, Gröndahl-Yli-Hannuksela K, Liukkonen J, Sorsa T, Suominen AL, Huumonen S, Könönen E
Publication year: 2017
Journal: Journal of Periodontal Research
Volume number: 52
Issue number: 3
Number of pages: 6
eISSN: 1600-0765


Background and Objective

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.

Material and Methods

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.

Last updated on 2019-21-08 at 22:04