Effect of MMP-1 promoter polymorphisms on GCF MMP-1 levels and outcome of periodontal therapy in patients with severe chronic periodontitis

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Abstract

Aims: The aims of this study were to investigate (1) the matrix metalloproteinase-1 (MMP-1) promoter polymorphisms in severe chronic periodontitis (CP), (2) the relationship of periodontal therapy outcome with these genotypes, and (3) the gingival crevicular fluid (GCF) MMP-1 levels-MMP-1 genotype correlation. Material and Methods: Genomic DNA was obtained from the peripheral blood of 102 patients with severe CP and 98 periodontally healthy subjects. MMP-1 -519AG and -1607 1G2G polymorphisms were determined by the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method. Fifty-eight CP patients received non-surgical periodontal therapy and were followed for 6 months. Clinical periodontal parameters and GCF samples were collected at baseline and at 6 months. GCF MMP-1 levels were analysed by enzyme-linked immunosorbent assay (ELISA). Results: The distribution of MMP-1 genotypes did not significantly differ between the study groups. On the other hand, the -1607 2G allele frequency of severe CP patients was higher than that of healthy subjects. MMP-1 -519G allele carriers had higher GCF MMP-1 levels and percentage of sites with 4-6 mm clinical attachment level (CAL) compared with AA genotypes after non-surgical periodontal therapy (p<0.05). Conclusions: These data suggest that the -1607 2G polymorphic allele of the MMP-1 gene could be associated with susceptibility to severe CP in the Turkish population. It seems that -519AG and GG genotypes could play a role in the outcome of periodontal therapy. © 2008 Blackwell Munksgaard.

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Pirhan, D., Atilla, G., Emingil, G., Sorsa, T., Tervahartiala, T., & Berdeli, A. (2008). Effect of MMP-1 promoter polymorphisms on GCF MMP-1 levels and outcome of periodontal therapy in patients with severe chronic periodontitis. Journal of Clinical Periodontology, 35(10), 862–870. https://doi.org/10.1111/j.1600-051X.2008.01302.x

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