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Isolation, Processing and Analysis of Murine Gingival Cells
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Mannose-binding lectin gene polymorphism in relation to periodontal infection
A Liukkonen1, Q He2, U K Gürsoy1
1Institute of Dentistry, University of Turku, Turku, Finland.
Journal of Periodontal Research
|September 15, 2016
Summary
Mannose-binding lectin (MBL) gene variants (MBL2) are linked to increased periodontal inflammation. MBL2 variants combined with Aggregatibacter actinomycetemcomitans infection worsen periodontitis markers.
Area of Science:
- Immunogenetics
- Periodontology
- Microbiology
Background:
- Mannose-binding lectin (MBL) is crucial for innate immunity.
- MBL deficiency often results from mutations in the MBL2 gene.
- MBL plays a role in the host's response to periodontal pathogens.
Purpose of the Study:
- To investigate MBL2 gene polymorphisms.
- To assess the relationship between MBL2 variants and salivary markers of periodontal inflammation and tissue destruction.
- To examine the association with periodontitis-associated bacteria: Aggregatibacter actinomycetemcomitans and Porphyromonas gingivalis.
Main Methods:
- Genotyping of MBL2 by pyrosequencing in 222 subjects (40-60 years old, ≥20 teeth).
- Subjects categorized into generalized periodontitis (80), localized periodontitis (65), and periodontitis-free (77) groups.
- Salivary analysis for A. actinomycetemcomitans, P. gingivalis, IL-1β, MMP-8, and TIMP-1 levels.
Main Results:
- MBL2 genotypes: A/A (69.4%), A/O (26.6%), O/O (4%).
- In A. actinomycetemcomitans-positive subjects with MBL2 variants (A/O or O/O), elevated IL-1β and decreased TIMP-1 were observed.
- These subjects also showed a higher MMP-8/TIMP-1 ratio and increased pocket teeth compared to those without A. actinomycetemcomitans.
Conclusions:
- MBL2 variants may predispose individuals to more severe periodontal inflammation and destruction.
- The presence of A. actinomycetemcomitans exacerbates periodontal disease in individuals with variant MBL2.
- This highlights the interplay between genetic predisposition and bacterial infection in periodontitis pathogenesis.
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