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Genetic Variations in the Human Gelatinase A (Matrix Metalloproteinase‐2) Promoter Are Not Associated With Susceptibility to, and Severity of, Chronic Periodontitis
Background: Gelatinase A (matrix metalloproteinase‐2 [MMP‐2]) has been shown to play an important role in the pathogenesis of several disorders, including periodontal diseases. In this study, we test the hypothesis that variations in this gene influence the development and severity of chronic period...
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Published in: | Journal of periodontology (1970) 2005-07, Vol.76 (7), p.1056-1060 |
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Main Authors: | , , , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that cite this one |
Online Access: | Get full text |
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Summary: | Background: Gelatinase A (matrix metalloproteinase‐2 [MMP‐2]) has been shown to play an important role in the pathogenesis of several disorders, including periodontal diseases. In this study, we test the hypothesis that variations in this gene influence the development and severity of chronic periodontitis.
Methods: Four promoter polymorphisms (‐1575G/A, ‐1306C/T, ‐790T/G, and ‐735C/T) were analyzed by polymerase chain reaction‐restriction fragment length polymorphism (PCR‐RFLP) methods in 149 patients with mild to severe chronic periodontitis and 127 age‐matched controls in the Czech population.
Results: No significant differences in distribution of the ‐1575G/A, ‐1306C/T, and ‐735C/T variants between periodontitis and control groups were detected in our study. However, a trend to decreased frequency of the ‐790 GG homozygotes was observed in patients with chronic periodontitis compared to healthy controls (P = 0.036, P corr >0.05). Haplotype analysis of four single nucleotide polymorphisms (SNP) in the MMP‐2 gene showed no significant association of any haplotype with chronic periodontitis.
Conclusion: Our findings suggest that polymorphisms in the MMP‐2 gene promoter do not contribute significantly to the interindividual periodontitis susceptibility and/or severity in European Caucasians, and they are not regulatory variants in this disease. J Periodontol 2005;76:1056‐1060. |
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ISSN: | 0022-3492 1943-3670 |
DOI: | 10.1902/jop.2005.76.7.1056 |